Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinary Tract Infection. This presentation contains real names of persons involve of this particular study. This names should not be copied or rewritten. Used the data of this study as basis only. All rights reserved 2009.
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinar...Jack Frost
The document presents a case study on a 37-year-old male patient, G.M., who was admitted to the hospital with complaints of lower extremity weakness. He was diagnosed with severe hypokalemia, hypoxic ischemic encephalopathy, nosocomial pneumonia, and a urinary tract infection. The patient experienced respiratory arrest and was intubated. He was treated with potassium supplements to address his hypokalemia and given antibiotics to treat his pneumonia and urinary tract infection. His conditions developed as complications during his hospital stay.
Hyperkalemia is defined as a plasma potassium level above 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space due to acidosis or medications, or inadequate renal excretion due to reduced aldosterone levels or impaired kidney function. Symptoms range from none to muscle weakness or paralysis to cardiac arrhythmias. ECG changes include peaked T waves and prolonged PR interval. Treatment involves calcium to stabilize the heart, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins, diuretics or hemodialysis to remove excess potassium.
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunting. It manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subtle alterations to coma. The main neurotoxin involved is ammonia, which is normally cleared by the liver. In liver disease, ammonia builds up in the blood and brain, where it interferes with neurotransmission. Symptoms include impaired cognition, personality changes, asterixis, and eventually coma. Hepatic encephalopathy is classified based on the underlying liver disease, time course, presence of precipitating factors, and severity of symptoms.
Hepatic encephalopathy is a condition characterized by confusion, changes in mental status, and coma caused by liver failure and resulting in the buildup of toxic substances normally removed by the liver. It is graded based on severity from mild confusion to coma. Common precipitants include renal failure, electrolyte imbalances, infections, and certain drugs. Diagnosis involves assessing liver function, ruling out other causes, and potentially measuring ammonia levels.
Uremic encephalopathy occurs when toxins that are normally cleared by the kidneys build up in the bloodstream due to kidney failure. It causes a range of neurological symptoms from mild issues like fatigue to severe problems like seizures and coma. The condition develops when kidney function declines to the point that creatinine clearance levels fall below 15 mL/min. While the exact cause is unknown, it involves the accumulation of various toxins in the brain that disrupts cell metabolism and function. Prompt treatment with dialysis or kidney transplantation can reverse the neurological symptoms.
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease and the accumulation of toxic metabolites like ammonia in the blood. It can progress from mild confusion to coma. Approximately 35% of cirrhosis patients die from hepatic coma. Causes include liver damage, infection, diuretics, and certain medications. Symptoms range from fatigue and irritability to confusion, disorientation and coma. Treatment focuses on removing causes and suppressing neurotoxin production via lactulose and antibiotics. Nursing care involves monitoring for symptoms, managing fluid balance and nutrition, preventing infections, and addressing risks like injury from loss of awareness.
Uremic Encephalopathy in End Stage Renal Disease A Case Reportijtsrd
This case report describes a 69-year-old male patient with end-stage renal disease who presented with neurological symptoms of uremic encephalopathy including slurred speech, muscle twitching, and weakness. The patient's symptoms improved with hemodialysis treatment. Uremic encephalopathy occurs when toxins accumulate in the brain due to kidney failure. Hemodialysis is effective at removing toxins and resolving associated neurological manifestations.
Dr Abdullah Ansari
PG-2 (Medicine)
AMU ALIGARH
A general approach to periodic paralysis....
(including hypokalemic periodic paralysis and thyrotoxic periodic paralysis, and other “Channelopathies” or “Membranopathies)
Pathophysiology
Epidemiology
Primary or familial periodic paralysis
Secondary periodic paralysis
Conventional classification of periodic paralysis
Classification of primary periodic paralysis based on ion-channel abnormalities
Clinical approach to a case of periodic paralysis
History of muscle weakness
Age of onset
Family history
Timing
Intensity
History of administration of certain drugs
Clinical examination
Differential Diagnosis
Laboratory investigations
Serum K+
CPK and serum myoglobin
ECG
EMG
Nerve conduction studies
Provocative Testing
Muscle biopsy
Treatment
Prognosis
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinar...Jack Frost
The document presents a case study on a 37-year-old male patient, G.M., who was admitted to the hospital with complaints of lower extremity weakness. He was diagnosed with severe hypokalemia, hypoxic ischemic encephalopathy, nosocomial pneumonia, and a urinary tract infection. The patient experienced respiratory arrest and was intubated. He was treated with potassium supplements to address his hypokalemia and given antibiotics to treat his pneumonia and urinary tract infection. His conditions developed as complications during his hospital stay.
Hyperkalemia is defined as a plasma potassium level above 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space due to acidosis or medications, or inadequate renal excretion due to reduced aldosterone levels or impaired kidney function. Symptoms range from none to muscle weakness or paralysis to cardiac arrhythmias. ECG changes include peaked T waves and prolonged PR interval. Treatment involves calcium to stabilize the heart, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins, diuretics or hemodialysis to remove excess potassium.
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunting. It manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subtle alterations to coma. The main neurotoxin involved is ammonia, which is normally cleared by the liver. In liver disease, ammonia builds up in the blood and brain, where it interferes with neurotransmission. Symptoms include impaired cognition, personality changes, asterixis, and eventually coma. Hepatic encephalopathy is classified based on the underlying liver disease, time course, presence of precipitating factors, and severity of symptoms.
Hepatic encephalopathy is a condition characterized by confusion, changes in mental status, and coma caused by liver failure and resulting in the buildup of toxic substances normally removed by the liver. It is graded based on severity from mild confusion to coma. Common precipitants include renal failure, electrolyte imbalances, infections, and certain drugs. Diagnosis involves assessing liver function, ruling out other causes, and potentially measuring ammonia levels.
Uremic encephalopathy occurs when toxins that are normally cleared by the kidneys build up in the bloodstream due to kidney failure. It causes a range of neurological symptoms from mild issues like fatigue to severe problems like seizures and coma. The condition develops when kidney function declines to the point that creatinine clearance levels fall below 15 mL/min. While the exact cause is unknown, it involves the accumulation of various toxins in the brain that disrupts cell metabolism and function. Prompt treatment with dialysis or kidney transplantation can reverse the neurological symptoms.
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease and the accumulation of toxic metabolites like ammonia in the blood. It can progress from mild confusion to coma. Approximately 35% of cirrhosis patients die from hepatic coma. Causes include liver damage, infection, diuretics, and certain medications. Symptoms range from fatigue and irritability to confusion, disorientation and coma. Treatment focuses on removing causes and suppressing neurotoxin production via lactulose and antibiotics. Nursing care involves monitoring for symptoms, managing fluid balance and nutrition, preventing infections, and addressing risks like injury from loss of awareness.
Uremic Encephalopathy in End Stage Renal Disease A Case Reportijtsrd
This case report describes a 69-year-old male patient with end-stage renal disease who presented with neurological symptoms of uremic encephalopathy including slurred speech, muscle twitching, and weakness. The patient's symptoms improved with hemodialysis treatment. Uremic encephalopathy occurs when toxins accumulate in the brain due to kidney failure. Hemodialysis is effective at removing toxins and resolving associated neurological manifestations.
Dr Abdullah Ansari
PG-2 (Medicine)
AMU ALIGARH
A general approach to periodic paralysis....
(including hypokalemic periodic paralysis and thyrotoxic periodic paralysis, and other “Channelopathies” or “Membranopathies)
Pathophysiology
Epidemiology
Primary or familial periodic paralysis
Secondary periodic paralysis
Conventional classification of periodic paralysis
Classification of primary periodic paralysis based on ion-channel abnormalities
Clinical approach to a case of periodic paralysis
History of muscle weakness
Age of onset
Family history
Timing
Intensity
History of administration of certain drugs
Clinical examination
Differential Diagnosis
Laboratory investigations
Serum K+
CPK and serum myoglobin
ECG
EMG
Nerve conduction studies
Provocative Testing
Muscle biopsy
Treatment
Prognosis
Cerebral edema and intracranial hypertension are major complications in patients with fulminant hepatic failure (FHF) and can lead to death. The pathophysiology of these complications involves changes in cerebral hemodynamics and metabolism that occur in progressive phases. Initially, cerebral blood flow is low due to low metabolic demand in the brain. Later, cerebral blood flow becomes excessive and uncoupled from metabolism, impairing autoregulation and decreasing intracranial pressure. This can ultimately lead to cerebral swelling and brain death if not reversed. The mechanisms underlying cerebral edema and hypertension in FHF are multi-factorial but involve astrocyte swelling due to ammonia and glutamine accumulation, disruption of the blood-brain barrier
This document discusses renal and hepatic encephalopathy. It defines uremic encephalopathy as a brain disorder that occurs in patients with untreated or inadequately treated kidney disease. Symptoms range from mild to severe and fluctuate depending on kidney function. Uremic toxins that accumulate due to renal dysfunction are a primary cause. Treatment involves optimizing dialysis to adequately remove toxins. Other types of encephalopathy discussed include dialysis dementia, central pontine myelinolysis, seizures, and restless leg syndrome. Causes, clinical features, diagnosis and management are described for each condition.
The document discusses hepatic encephalopathy, a neurological syndrome caused by liver dysfunction. It covers the pathogenesis, which involves neurotoxins like ammonia crossing the blood brain barrier and disrupting neurotransmitter levels. Symptoms range from mild confusion to coma and can be precipitated by factors that increase ammonia production or permeability of the blood brain barrier. Treatment focuses on managing precipitating factors and restricting protein intake to control ammonia levels.
This document discusses hyperkalemia (high potassium levels), including its causes, effects on the heart, diagnosis, and treatment. It describes a case report of a 69-year-old woman who experienced hyperkalemia after dialysis. Her symptoms included abdominal pain, fatigue, and arrhythmia. Treatment involved calcium, insulin, glucose, and emergent dialysis to lower her potassium level. The document then provides details on potassium regulation in the body, effects of high potassium on heart function, electrocardiogram changes seen with hyperkalemia, common causes, and approaches for treating acute hyperkalemia including membrane stabilization, promoting potassium influx, and potassium removal methods like dialysis or sodium polystyrene sulfonate.
This document outlines a presentation on hepatic encephalopathy. It begins with an introduction defining hepatic encephalopathy and its clinical spectrum. It then covers the epidemiology, classification, etiopathogenesis including theories around ammonia and GABA, clinical features, differential diagnosis, investigations including blood tests and EEG, and treatment including lactulose, antibiotics, and dietary changes. The presentation concludes with references.
This document discusses the management of hyperkalemia in chronic kidney disease (CKD). It notes that hyperkalemia is common in CKD patients, affecting 40-50% of those with end-stage renal disease, and is associated with increased mortality. The causes of hyperkalemia in CKD include increased intracellular shifting of potassium, decreased renal excretion, and medications that inhibit the renin-angiotensin-aldosterone system. The document outlines approaches for acute and chronic management of hyperkalemia in CKD, including calcium supplementation, insulin therapy, beta-agonists, cation exchange resins, and dialysis in severe cases. It emphasizes the importance of addressing both acute life-threatening rises in potassium as well
Hyponatremia in neurological patients: cerebral salt wasting versus inappropr...Amit Agrawal
This document discusses hyponatremia in neurological patients, specifically comparing cerebral salt wasting syndrome (CSW) and syndrome of inappropriate antidiuretic hormone secretion (SIADH). It notes that hyponatremia is common in acute neurological patients and can worsen outcomes. The key difference between CSW and SIADH is volume status, which is difficult to assess, though treatment differs with fluid restriction for SIADH and saline replacement for CSW. Correct diagnosis and management of hyponatremia in these patients is important.
This document presents a case of a 52-year-old female with fluid and electrolyte imbalance. She was admitted for shortness of breath and found to have hyponatremia and pulmonary congestion secondary to heart failure. Laboratory results showed low sodium, high BUN, and abnormal electrolyte ratios. She was diagnosed with hypervolemic hyponatremia and treated with diuretics and fluid restriction, resulting in improved sodium levels over five days. The document then discusses key principles of fluid balance, electrolytes, hypovolemia, and their management.
Management of hyperkalemia dakahlia medical syndicate 2o18FAARRAG
This document discusses hyperkalemia (high potassium levels), including its definition, classification, causes, and approach to assessment and management. Some key points:
- Hyperkalemia is defined as a serum potassium level above 5.0-5.5 mEq/L in adults and can be mild (5.5-6.0 mEq/L), moderate (6.1-7.0 mEq/L), or severe (≥7.0 mEq/L). Levels over 7-8.5 mEq/L can cause cardiac issues.
- Causes include reduced renal excretion, shifts of potassium from cells to blood, and excessive potassium intake. Patients with kidney disease or
Hepatic encephalopathy is a brain disorder caused by liver impairment that results in toxic substances not being removed from the blood. This causes disturbances in mental functioning. It is commonly seen in people with cirrhosis when substances like ammonia accumulate abnormally in the blood and reach the brain. Symptoms range from mood changes to confusion and coma depending on severity. Treatment focuses on restricting diet to reduce toxic substances in the intestines and administering medications to promote bowel movements and removal of toxins from the blood. For severe cases, hospitalization, ventilator support, artificial liver support, or even liver transplantation may be needed.
A blockage of blood flow to the heart muscle.
A heart attack is a medical emergency. A heart attack usually occurs when a blood clot blocks blood flow to the heart. Without blood, tissue loses oxygen and dies.
Symptoms include tightness or pain in the chest, neck, back or arms, as well as fatigue, lightheadedness, abnormal heartbeat and anxiety. Women are more likely to have atypical symptoms than men.
Treatment ranges from lifestyle changes and cardiac rehabilitation to medication, stents and bypass surgery.
Cerebral salt wasting syndrome (CSWS) is a condition where there is renal loss of sodium during intracranial disorders leading to hyponatremia. It is commonly caused by subarachnoid hemorrhage, brain injuries, or central nervous system infections. CSWS results from disruption of hypothalamic-renal pathways and an imbalance of sympathetic output. Patients experience hyponatremia and a decrease in extracellular fluid volume. Treatment involves slow sodium and water replacement to correct the hyponatremia while avoiding too rapid of a correction which can cause cerebral edema.
Elderly patients represent the fastest growing population globally. They experience many age-related physiological changes that increase surgical risk. Preoperative evaluation and optimization is important to identify risks like cardiovascular disease and pulmonary issues. Anesthesia in the elderly requires lower doses of induction agents and opioids due to pharmacokinetic changes. Regional anesthesia may provide benefits over general anesthesia. Close postoperative monitoring is needed due to risks of complications like delirium, cognitive dysfunction, hypotension, and hypothermia.
This document discusses neonatal shock, including its pathophysiology, terminology, history of inotropic drugs, and clinical uses of various inotropic agents. It covers topics such as the unique features of the preterm cardiovascular system, oxygen delivery principles, shock etiologies like hypovolemia and myocardial dysfunction, and the mechanisms and receptors targeted by drugs like dopamine, dobutamine, epinephrine, norepinephrine, milrinone, vasopressin, and corticosteroids. Clinical scenarios where different agents may be beneficial or have limitations are also summarized.
An electrolyte disorder occurs when there is an imbalance in ionized salts like sodium, potassium, calcium, and magnesium in the blood. Electrolytes help regulate pH, fluid balance, and neuromuscular and organ function. Common electrolyte disorders include hypernatremia, hyponatremia, hyperkalemia, hypokalemia, hypercalcemia, and hypocalcemia. Treatment involves identifying the cause, restricting intake of the abnormal electrolyte, and slowly correcting the imbalance to avoid complications like cerebral edema.
Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
Hypokalemic Periodic Paralysis A Case Reportijtsrd
"Hypokalemic periodic paralysis HPP is a medical emergency with prevalence of 1 in 100,000 . Rapid management is very important since, very low potassium levels can lead to cardiac complications . In this case, a twenty four year old female without a similar history in the family, having hypokalemia periodic paralysis attack is presented. This case report study has been presented for the consideration of the rare HPP in patients presenting with sudden muscle weakness. Blessy Rachal Boban | Cillamol K. J | Elena Cheruvil | Sheffin Thomas | Tony Abraham ""Hypokalemic Periodic Paralysis: A Case Report"" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-3 | Issue-3 , April 2019, URL: https://www.ijtsrd.com/papers/ijtsrd21658.pdf
Paper URL: https://www.ijtsrd.com/pharmacy/pharmacy-practice/21658/hypokalemic-periodic-paralysis-a-case-report/blessy-rachal-boban"
AKI in neonates can be caused by prerenal, intrinsic renal, or postrenal factors. It is defined and classified using creatinine and urine output criteria. Management involves identifying and treating the underlying cause, maintaining fluid/electrolyte balance, and considering renal replacement therapy for refractory cases. Peritoneal dialysis is often preferred for neonates as it is gentler than hemodialysis and can provide both fluid removal and metabolic control. However, peritoneal dialysis also carries risks of peritonitis, mechanical issues, and complications in critically ill infants.
This document discusses hypertension (high blood pressure) and ischemia-reperfusion injury. It defines hypertension and describes its different types, including essential and secondary hypertension. It also outlines blood pressure classifications. The document then defines ischemia as restricted blood supply and ischemia-reperfusion injury as tissue damage caused when blood supply returns after ischemia. It lists conditions where ischemia-reperfusion injury occurs and cellular changes during ischemia. Therapeutic interventions targeting ischemia-reperfusion injury are also discussed, along with preconditioning to increase resistance to loss of blood supply.
Cerebral edema and intracranial hypertension are major complications in patients with fulminant hepatic failure (FHF) and can lead to death. The pathophysiology of these complications involves changes in cerebral hemodynamics and metabolism that occur in progressive phases. Initially, cerebral blood flow is low due to low metabolic demand in the brain. Later, cerebral blood flow becomes excessive and uncoupled from metabolism, impairing autoregulation and decreasing intracranial pressure. This can ultimately lead to cerebral swelling and brain death if not reversed. The mechanisms underlying cerebral edema and hypertension in FHF are multi-factorial but involve astrocyte swelling due to ammonia and glutamine accumulation, disruption of the blood-brain barrier
This document discusses renal and hepatic encephalopathy. It defines uremic encephalopathy as a brain disorder that occurs in patients with untreated or inadequately treated kidney disease. Symptoms range from mild to severe and fluctuate depending on kidney function. Uremic toxins that accumulate due to renal dysfunction are a primary cause. Treatment involves optimizing dialysis to adequately remove toxins. Other types of encephalopathy discussed include dialysis dementia, central pontine myelinolysis, seizures, and restless leg syndrome. Causes, clinical features, diagnosis and management are described for each condition.
The document discusses hepatic encephalopathy, a neurological syndrome caused by liver dysfunction. It covers the pathogenesis, which involves neurotoxins like ammonia crossing the blood brain barrier and disrupting neurotransmitter levels. Symptoms range from mild confusion to coma and can be precipitated by factors that increase ammonia production or permeability of the blood brain barrier. Treatment focuses on managing precipitating factors and restricting protein intake to control ammonia levels.
This document discusses hyperkalemia (high potassium levels), including its causes, effects on the heart, diagnosis, and treatment. It describes a case report of a 69-year-old woman who experienced hyperkalemia after dialysis. Her symptoms included abdominal pain, fatigue, and arrhythmia. Treatment involved calcium, insulin, glucose, and emergent dialysis to lower her potassium level. The document then provides details on potassium regulation in the body, effects of high potassium on heart function, electrocardiogram changes seen with hyperkalemia, common causes, and approaches for treating acute hyperkalemia including membrane stabilization, promoting potassium influx, and potassium removal methods like dialysis or sodium polystyrene sulfonate.
This document outlines a presentation on hepatic encephalopathy. It begins with an introduction defining hepatic encephalopathy and its clinical spectrum. It then covers the epidemiology, classification, etiopathogenesis including theories around ammonia and GABA, clinical features, differential diagnosis, investigations including blood tests and EEG, and treatment including lactulose, antibiotics, and dietary changes. The presentation concludes with references.
This document discusses the management of hyperkalemia in chronic kidney disease (CKD). It notes that hyperkalemia is common in CKD patients, affecting 40-50% of those with end-stage renal disease, and is associated with increased mortality. The causes of hyperkalemia in CKD include increased intracellular shifting of potassium, decreased renal excretion, and medications that inhibit the renin-angiotensin-aldosterone system. The document outlines approaches for acute and chronic management of hyperkalemia in CKD, including calcium supplementation, insulin therapy, beta-agonists, cation exchange resins, and dialysis in severe cases. It emphasizes the importance of addressing both acute life-threatening rises in potassium as well
Hyponatremia in neurological patients: cerebral salt wasting versus inappropr...Amit Agrawal
This document discusses hyponatremia in neurological patients, specifically comparing cerebral salt wasting syndrome (CSW) and syndrome of inappropriate antidiuretic hormone secretion (SIADH). It notes that hyponatremia is common in acute neurological patients and can worsen outcomes. The key difference between CSW and SIADH is volume status, which is difficult to assess, though treatment differs with fluid restriction for SIADH and saline replacement for CSW. Correct diagnosis and management of hyponatremia in these patients is important.
This document presents a case of a 52-year-old female with fluid and electrolyte imbalance. She was admitted for shortness of breath and found to have hyponatremia and pulmonary congestion secondary to heart failure. Laboratory results showed low sodium, high BUN, and abnormal electrolyte ratios. She was diagnosed with hypervolemic hyponatremia and treated with diuretics and fluid restriction, resulting in improved sodium levels over five days. The document then discusses key principles of fluid balance, electrolytes, hypovolemia, and their management.
Management of hyperkalemia dakahlia medical syndicate 2o18FAARRAG
This document discusses hyperkalemia (high potassium levels), including its definition, classification, causes, and approach to assessment and management. Some key points:
- Hyperkalemia is defined as a serum potassium level above 5.0-5.5 mEq/L in adults and can be mild (5.5-6.0 mEq/L), moderate (6.1-7.0 mEq/L), or severe (≥7.0 mEq/L). Levels over 7-8.5 mEq/L can cause cardiac issues.
- Causes include reduced renal excretion, shifts of potassium from cells to blood, and excessive potassium intake. Patients with kidney disease or
Hepatic encephalopathy is a brain disorder caused by liver impairment that results in toxic substances not being removed from the blood. This causes disturbances in mental functioning. It is commonly seen in people with cirrhosis when substances like ammonia accumulate abnormally in the blood and reach the brain. Symptoms range from mood changes to confusion and coma depending on severity. Treatment focuses on restricting diet to reduce toxic substances in the intestines and administering medications to promote bowel movements and removal of toxins from the blood. For severe cases, hospitalization, ventilator support, artificial liver support, or even liver transplantation may be needed.
A blockage of blood flow to the heart muscle.
A heart attack is a medical emergency. A heart attack usually occurs when a blood clot blocks blood flow to the heart. Without blood, tissue loses oxygen and dies.
Symptoms include tightness or pain in the chest, neck, back or arms, as well as fatigue, lightheadedness, abnormal heartbeat and anxiety. Women are more likely to have atypical symptoms than men.
Treatment ranges from lifestyle changes and cardiac rehabilitation to medication, stents and bypass surgery.
Cerebral salt wasting syndrome (CSWS) is a condition where there is renal loss of sodium during intracranial disorders leading to hyponatremia. It is commonly caused by subarachnoid hemorrhage, brain injuries, or central nervous system infections. CSWS results from disruption of hypothalamic-renal pathways and an imbalance of sympathetic output. Patients experience hyponatremia and a decrease in extracellular fluid volume. Treatment involves slow sodium and water replacement to correct the hyponatremia while avoiding too rapid of a correction which can cause cerebral edema.
Elderly patients represent the fastest growing population globally. They experience many age-related physiological changes that increase surgical risk. Preoperative evaluation and optimization is important to identify risks like cardiovascular disease and pulmonary issues. Anesthesia in the elderly requires lower doses of induction agents and opioids due to pharmacokinetic changes. Regional anesthesia may provide benefits over general anesthesia. Close postoperative monitoring is needed due to risks of complications like delirium, cognitive dysfunction, hypotension, and hypothermia.
This document discusses neonatal shock, including its pathophysiology, terminology, history of inotropic drugs, and clinical uses of various inotropic agents. It covers topics such as the unique features of the preterm cardiovascular system, oxygen delivery principles, shock etiologies like hypovolemia and myocardial dysfunction, and the mechanisms and receptors targeted by drugs like dopamine, dobutamine, epinephrine, norepinephrine, milrinone, vasopressin, and corticosteroids. Clinical scenarios where different agents may be beneficial or have limitations are also summarized.
An electrolyte disorder occurs when there is an imbalance in ionized salts like sodium, potassium, calcium, and magnesium in the blood. Electrolytes help regulate pH, fluid balance, and neuromuscular and organ function. Common electrolyte disorders include hypernatremia, hyponatremia, hyperkalemia, hypokalemia, hypercalcemia, and hypocalcemia. Treatment involves identifying the cause, restricting intake of the abnormal electrolyte, and slowly correcting the imbalance to avoid complications like cerebral edema.
Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
Hypokalemic Periodic Paralysis A Case Reportijtsrd
"Hypokalemic periodic paralysis HPP is a medical emergency with prevalence of 1 in 100,000 . Rapid management is very important since, very low potassium levels can lead to cardiac complications . In this case, a twenty four year old female without a similar history in the family, having hypokalemia periodic paralysis attack is presented. This case report study has been presented for the consideration of the rare HPP in patients presenting with sudden muscle weakness. Blessy Rachal Boban | Cillamol K. J | Elena Cheruvil | Sheffin Thomas | Tony Abraham ""Hypokalemic Periodic Paralysis: A Case Report"" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-3 | Issue-3 , April 2019, URL: https://www.ijtsrd.com/papers/ijtsrd21658.pdf
Paper URL: https://www.ijtsrd.com/pharmacy/pharmacy-practice/21658/hypokalemic-periodic-paralysis-a-case-report/blessy-rachal-boban"
AKI in neonates can be caused by prerenal, intrinsic renal, or postrenal factors. It is defined and classified using creatinine and urine output criteria. Management involves identifying and treating the underlying cause, maintaining fluid/electrolyte balance, and considering renal replacement therapy for refractory cases. Peritoneal dialysis is often preferred for neonates as it is gentler than hemodialysis and can provide both fluid removal and metabolic control. However, peritoneal dialysis also carries risks of peritonitis, mechanical issues, and complications in critically ill infants.
This document discusses hypertension (high blood pressure) and ischemia-reperfusion injury. It defines hypertension and describes its different types, including essential and secondary hypertension. It also outlines blood pressure classifications. The document then defines ischemia as restricted blood supply and ischemia-reperfusion injury as tissue damage caused when blood supply returns after ischemia. It lists conditions where ischemia-reperfusion injury occurs and cellular changes during ischemia. Therapeutic interventions targeting ischemia-reperfusion injury are also discussed, along with preconditioning to increase resistance to loss of blood supply.
Metabolic disoders internal medicine and neuroscienceNeilVincentDeAsis
This document discusses acquired metabolic disorders of the nervous system that result from failure of other organ systems. It focuses on hypoxic-ischemic encephalopathy, where lack of oxygen and blood flow to the brain causes global disturbance of cerebral function. The main causes are discussed as well as the clinical features and progression from confusion to stupor and coma. Laboratory tests that can help identify potential causes are also outlined.
Shock is defined as inadequate tissue perfusion resulting in decreased oxygenation at the cellular level. The document classifies shock into four types: cardiogenic, hypovolemic, obstructive, and distributive. Signs of shock include extremely low blood pressure, weakness, rapid breathing, and loss of consciousness. Treatment involves pharmacological interventions like inotropic drugs and fluid resuscitation as well as non-pharmacological measures like oxygen supplementation.
Shock is a state of low tissue perfusion that can be fatal if not treated promptly. There are several types of shock based on the underlying pathophysiology, including hypovolaemic shock (from blood or fluid loss), cardiogenic shock (from heart failure), distributive shock (from sepsis or anaphylaxis), and obstructive shock (from embolism or pulmonary hypertension). Early resuscitation is crucial and involves restoring circulating volume through intravenous fluids while also identifying and treating the underlying cause of shock. Outcomes depend on limiting the duration of tissue hypoperfusion to prevent multiple organ failure.
This document provides an overview of hepatic encephalopathy. It begins by defining hepatic encephalopathy as brain dysfunction caused by liver insufficiency, manifesting as neurological or psychiatric abnormalities ranging from subtle changes to coma. It then covers classifications, pathogenesis involving toxins like ammonia, diagnosis through clinical features and lab tests, treatment primarily with non-absorbable disaccharides like lactulose to reduce ammonia, and prognosis which can include coma and death for chronic or severe cases.
This document provides a summary of fluid and electrolyte management, focusing on disorders of potassium homeostasis (hypokalemia and hyperkalemia) and their pathophysiology, clinical features, diagnosis, and management.
Key points include:
- Gastroenteritis is a common cause of pediatric hypokalemia. Treatment involves oral or IV potassium replacement depending on severity.
- Symptomatic or severe hyperkalemia requires three steps - cardiac protection with calcium, promoting intracellular shifts with insulin/glucose, and enhancing excretion with medications.
- Pseudohyperkalemia can cause falsely elevated potassium levels and must be ruled out with a new blood draw.
- Specific ECG changes
This document provides information about hyperglycemic hyperosmolar syndrome (HHS), including other names for the condition, definitions, pathophysiology, diagnostic tests, treatment, complications, nursing diagnoses, and more. HHS is a life-threatening emergency caused by severe hyperglycemia and lack of insulin. It is characterized by extremely high blood glucose levels over 400 mg/dL, hyperosmolality due to water loss from cells, and lack of ketosis. Diagnostic tests show electrolyte imbalances. Treatment focuses on rapid fluid replacement and slow insulin administration to lower blood glucose levels over 24-48 hours. Complications can include organ failure, infection, and death if not properly treated.
Refeeding syndrome occurs when malnourished patients begin eating again and can cause dangerous shifts in fluid, electrolyte, and nutrient balance. Key risks include hypophosphatemia, hypokalemia, hypomagnesia, and thiamine deficiency. Left untreated, refeeding syndrome can lead to complications affecting multiple organ systems like the heart, lungs, blood, liver and nerves. Prevention methods include slowly increasing calorie intake, correcting electrolyte imbalances, and supplementing with phosphorus, potassium, magnesium and thiamine during the refeeding period.
Diabetic ketoacidosis is a life-threatening complication of diabetes that occurs when there is not enough insulin in the body. It is characterized by high blood sugars, high ketones, and metabolic acidosis. The main treatment involves fluid replacement, insulin therapy to lower blood sugars and ketones, correcting electrolyte imbalances like potassium, and treating any underlying infections. Complications can include hypokalemia, hypoglycemia, cerebral edema, and pulmonary edema. Patient education focuses on medication adherence, sick-day management, and seeking medical care if symptoms worsen.
This document discusses shock, including its definition, pathophysiology, classification, and severity. Shock is defined as a state of inadequate tissue perfusion resulting from reduced cardiac output, blood loss, or vascular dysfunction. The main types are hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The pathophysiology involves cellular hypoxia, inflammation, microvascular dysfunction, and ischemia-reperfusion injury. More severe shock is characterized by worsening metabolic acidosis, hypotension, oliguria, and loss of consciousness. Early recognition and treatment of compensated shock is important to prevent multi-organ failure.
This document discusses potassium imbalance, specifically hypokalemia and hyperkalemia. It defines hypokalemia as a potassium level below 3.5 mmol/L and hyperkalemia as above 5.0 mmol/L. For hypokalemia, it describes causes such as redistribution of potassium or renal/nonrenal losses. Signs include cardiac arrhythmias and muscle weakness. For hyperkalemia, it lists causes like increased intake, intracellular shifting, or decreased excretion. Evaluation involves ECG and lab tests. Management focuses on stabilizing cardiac function and promoting potassium excretion or shifting.
Perinatal asphyxia refers to progressive hypoxia, hypercarbia and acidosis during birth. It can cause multi-organ dysfunction in neonates. The essential criteria for diagnosis are prolonged acidemia on cord blood, low Apgar scores for over 5 minutes, and neurological or multi-organ issues in the newborn period. Asphyxia is caused by factors that limit oxygen delivery to the fetus, such as placental insufficiency, cord accidents, difficult delivery, or postnatal cardiac or respiratory issues. The brain, heart, kidneys and lungs are most commonly affected. Treatment involves resuscitation, controlling seizures, avoiding hyperthermia, and therapeutic hypothermia within 6 hours of birth to reduce neurological
This document provides an overview of hypoxic ischemic encephalopathy (HIE) with a focus on recent advances. It defines key terms related to oxygen deprivation and discusses the pathophysiology of HIE including cerebral blood flow disruption, excitotoxicity, oxidative stress, inflammation, and apoptosis. The document outlines risk factors, etiologies, and neurological patterns of injury for HIE. It also covers the diagnosis of HIE including clinical assessment, laboratory tests, neurologic signs, and staging systems.
This document provides an overview of the principles of shock management. It defines shock and describes its causes, including hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. The stages of shock - non-progressive, progressive decompensated, and decompensated - are outlined. Signs and symptoms of shock are provided. Finally, the document discusses the general management of shock, which aims to improve oxygen delivery and utilization to prevent organ injury through restoration of perfusion and supportive care.
This document discusses different types of shock including hypovolemic, septic, cardiogenic, neurogenic, and anaphylactic shock. It provides details on the definition, pathophysiology, clinical presentation, risk factors, and management of each type. For hypovolemic shock, it further discusses classification, fluid resuscitation, indicators of successful resuscitation, and choice of crystalloid versus colloid fluids. Septic shock is emphasized as an important type that can lead to multiple organ failure.
This document discusses congestive heart failure (CHF), including its definition, causes, pathophysiology, clinical manifestations, diagnosis, and management. CHF is characterized by inadequate systemic perfusion due to cardiac abnormalities. The most common cause is left ventricular systolic dysfunction. Clinical manifestations include dyspnea, edema, fatigue, and reduced exercise tolerance. Diagnosis involves imaging, labs, and assessing symptoms according to the NYHA classification system. Management focuses on controlling congestion with diuretics, enhancing contractility with drugs like digoxin, preventing worsening with ACE inhibitors and beta blockers, and treating the underlying cause.
Hypoxic Ischemic Encephalopathy (HIE) occurs when a term infant experiences intrapartum asphyxia and lack of oxygen. It can lead to death or disabilities like cerebral palsy. Diagnosis involves assessing the infant at birth using the APGAR score and neurological staging. Imaging tools like MRI are useful for showing patterns of brain injury. HIE management aims to prevent further brain damage through measures like temperature control and treating seizures, while newer treatments target excitotoxicity and oxidative stress.
Hypoxic Ischemic Encephalopathy (HIE) occurs when a term infant experiences intrapartum asphyxia and lack of oxygen. It can cause death or disabilities like cerebral palsy. Diagnosis involves assessing the infant at birth using the APGAR score and neurological staging. Imaging tools like MRI are useful to detect brain injury patterns. HIE management aims to prevent further brain damage through temperature control, seizure treatment, and potentially neuroprotective drugs. The condition remains a major cause of newborn mortality and morbidity.
Similar to Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinary Tract Infection (20)
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Important Names And Dates for Canadian Citizenship ExamJack Frost
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The document outlines notes and replays from a 27-day e-commerce challenge, providing links to video presentations on topics like finding winning products, setting up Shopify stores, Facebook advertising, outsourcing, and generating sales. Each day covers a different e-commerce topic presented by experts like Chris Record, Damien Coughlan, and Lawrence Aponte to teach strategies for building successful Shopify stores.
This patient has multiple chronic conditions including diabetes, COPD, cirrhosis, and a history of blood clots. Their home medication regimen includes over a dozen regularly scheduled medications across several drug classes to manage these conditions, as well as PRN medications for pain, nausea, and bowel issues. Non-compliance with this complex regimen could seriously impact the patient's health.
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This document contains information about various medical terms organized into 6 categories. It provides definitions for terms related to medications, vitamins, medical tests, surgical procedures, and more. Key details include definitions of medications used to treat allergies, nausea, hypothyroidism, and infections. It also defines terms like enhanced recovery after surgery protocol, dermatome assessment, and nephrostomy tube.
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LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
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land.
The utilization of land is impacted by human needs and environmental factors. In countries
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Therefore, human intervention has significantly influenced land use patterns over many
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providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
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and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
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Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinary Tract Infection
1. Velez College – College of Nursing
F. Ramos St., Cebu City
Presented by: Dave Jay S. Manriquez, RN.
A Case Study Presentation on G.M., Diagnosed with Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinary Tract Infection
INTRODUCTION:
G.M., 37 y.o., M, was admitted for the first time at CVGH Hospital on November 24, 2006, 7:00 pm via taxi, accompanied by his co-workers under the services of
he Department of Family Medicine, co-managed with the Department of Internal Medicine for complaints of lower extremity weakness noted hours PTA.
HYPOKALEMIA
Definition
Hypokalemia is a condition of below normal levels of potassium in the blood serum. Potassium is a necessary electrolyte which facilitates nerve impulse
conduction and the contraction of skeletal and smooth muscles, including the heart. It also facilitates cell membrane function and proper enzyme activity. Nearly 98% of
the body's potassium is intracellular. Levels must be kept in a proper (homeostatic) balance for the maintenance of health. The kidney determines potassium homeostasis,
and excess potassium is excreted in the urine.
The normal concentration of potassium in the serum is in the range of 3.5-5.0 mEq/L, thus, hypokalemia means serum or plasma levels of potassium ions that fall
below 3.5 mEq/L. Moderate hypokalemia is a serum level of 2.5-3 mEq/L, and severe hypokalemia is defined as a level less than 2.5 mEq/L The patient’s potassium
level is 1.5 meq/L, and is classified as severe.
Symptoms
Mild hypokalemia usually results in no symptoms, while moderate hypokalemia results in: confusion, disorientation, weakness, and discomfort of muscles. It also
causes cramps during exercise, and a discomfort in the legs experienced while sitting still. Severe hypokalemia results in: extreme weakness of the body, and occasionally
in paralysis, which occurs as quot;flaccid paralysisquot; or limpness. The symptoms manifested by the patient was the weakness of his lower extremities hours prior to
admission. Paralysis of the muscles of the lungs results in death. Our patient persistently complained of dyspnea, though pulse oximetry revealed 98-100%. Patient
experienced respiratory arrest, on his first day at the ICU, and was intubated with continuous ambubagging at 10 LPM. Another dangerous result is abnormal heart beat
(arrhythmia) that can lead to death from cardiac arrest (cessation of heart beat), because of the need for potassium to control muscle action. Mild QRS complexes were
documented in ECG. Along the course of intubation, patient went into cardiopulmonary arrest and was resuscitated accordingly.
2. Causes
The most common cause is by the use of diuretics, drugs that increase the excretion of water and salts in the urine. These are used to treat medical conditions,
including hypertension (high blood pressure), congestive heart failure, liver disease, and kidney disease. However, its side effects produce hypokalemia, the most
common cause of hypokalemia in elderly patients.
Another common cause is excessive diarrhea and / or vomiting. These can be produced by infections of the gastrointestinal tract. Diarrhea is a major world health
problem, responsible for about a quarter of the 10 million deaths that occur each year. in the parts of Asia and Africa. This also results in various abnormalities or
complications, such as dehydration (loss in body water), hyponatremia (low sodium level in the blood), and hypokalemia. Diarrhea was the identified cause of the
patient’s hypokalemia, who experienced diarrhea, with 10 episodes per day, amounting to 1 cup per episode. No meds were taken nor hydration to correct his condition.
His diarrhea was said to be acquired from eating seafood in Cebu.
Vomiting provokes an increase in potassium loss in the urine. Vomiting expels acid from the mouth, and this loss of acid results in alkalization of the blood. (pH
of the blood increases slightly.) An increased blood pH has a direct effect on the kidneys. Alkaline blood provokes the kidneys to release excessive amounts of potassium
in the urine. So, severe and continual vomiting can cause excessive losses of potassium from the body and hypokalemia.
Prolonged fasting and starvation also declines the blood serum potassium levels to below 3.0 mEq/L. But eating an unbalanced diet does not cause hypokalemia
because most foods, such as fruits (especially bananas, oranges, and melons), vegetables, meat, milk, and cheese, are good sources of potassium. Only foods such as
butter, margarine, vegetable oil, soda water, jelly beans, and hard candies are extremely poor in potassium.
Diagnosis
Hypokalemia can be measured by acquiring a sample of blood, to measure the concentration of potassium ions. Another way is by measuring the potassium
content of the urine. In the patient’s case, the serum potassium was measured with the value 1.5 meq/L(3.5-5meq/L). The electrocardiogram is also useful in the
diagnosis of hypokalemia, since hypokalemia results in abnormalities in heart behavior. ECG changes may be helpful if present, their absence should not be taken as
reassurance of normal cardiac conduction. The ECG of the patient showed mild QRS complexes.
Medical Management
Asymptomatic or mild hypokalemia may be treated with enteral potassium supplements in the form of pills. This is the safest and most effective treatment for
hypokalemia. Symptomatic or severe hypokalemia should be corrected with a solution of intravenous potassium. For people taking diuretics, potassium supplements are
not necessary as long as they eat a balanced diet containing foods rich in potassium. But if hypokalemia has already occurred, use of the high potassium diet alone may
not reverse hypokalemia. The treatment of the patient’s hypokalemia consisted of kalium durule (C: mineral and electrolyte replacement or supplement; A: replaces
potassium and maintains potassium level , 2 durules TID per NGT.
Surgical Management
Management is nonsurgical. Medical therapy is aimed at potassium supplementation by the enteral (ie, oral or through feeding tubes) or parenteral route.
Potassium supplements restore body potassium storage. Electrolytes are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance and to
reestablish osmotic equilibrium of specific ion..
3. HYPOXIC-ISCHEMIC ENCEPHALOPATHY
Definition
This is a serious condition causing significant mortality and long-term morbidity. HIE is characterized by clinical and laboratory evidence of acute or subacute
brain injury due to asphyxia (ie, hypoxia, acidosis). This damages the cells in the central nervous system (the brain and spinal cord) from inadequate oxygen. Most often,
the underlying cause remains unknown. Hypoxic-ischemic encephalopathy allegedly may cause in death or result in what is later recognized as developmental delay,
mental retardation, or cerebral palsy. The time of brain injury often remains uncertain, and an abnormal brain (eg, growth failure, impaired development) might be an
underlying risk factor.
Symptoms
May show symptoms of developmental delay, mental retardation, cerebral palsy and growth failure.
Causes
Brain hypoxia and ischemia due to systemic hypoxemia, reduced cerebral blood flow or both are the primary physiological processes that trigger HIE. A possible
cause in the patient’s case is the occurrence of respiratory arrest, secondary to weakness of respiratory muscles while he was in the ICU, leading to the lack of delivery of
oxygen to the brain. He complained of dyspnea, and metabolic acidosis was revealed.
Diagnosis
Diagnosis of HIE is made based on the history and physical and neurological examinations. Many of the tests are performed to assess the severity of brain injury
and to monitor the functional status of systemic organs. The results of the tests should be interpreted in conjunction with the clinical history and the findings from physical
examination. Cranial ultrasound can also reveal internal hemorrhage; however, visualizations may be difficult in routine ultrasound examination. A CT scan of the head
can be useful to confirm cerebral edema (obliteration of cerebral ventricles, blurring of sulci). Echocardiography (ECHO) also helps to define myocardial contractility and
the existence of structural heart defects, if any.
Medical Management
Seizures are generally self-limited, but may significantly compromise other body functions such as maintenance of ventilation, oxygenation, and blood pressure.
Seizures should be treated early and be well controlled, since even asymptomatic seizures (ie, seen only on EEG) may continue to injure the brain. Fluid and glucose
homeostasis should also be achieved. Avoid hypoglycemia or hyperglycemia, as both are known to cause brain injury. Treatment is supportive and directed at the organ
system manifestations. For the brain injury, no established effective treatment is used. Citicoline (Somazine) can be used as a neuroprotectant(C: CNS stimulant; A: it
produces CNS stimulation by increasing level of neurotransmitters in the CNS. Produce CNS stimulation and respiratory stimulation dilated pupils, increase motor
activity and mental alertness, and a diminished sense of fatigue.); .
Surgical Management
In cases of posterior cranial fossa hematoma, surgical drainage may be lifesaving if no additional pathologies are present
4. NOSOCOMIAL PNEUMONIA
Definition
Hospital-acquired pneumonia, also called nosocomial pneumonia, is an infection that patients get while they’re in the hospital. This means the infection is
not present at the time a patient is admitted to the hospital. Pathogens thrive in hospitals that could not survive in other environments. These pathogens include
resistent aerobic gram-negative rods, such as Pseudomonas, Enterobacter and Serratia; resistent gram positive cocci, such as ORSA. Because of risk factors,
underlying morbidity and resistent bacteria, hospital-acquired pneumonia tends to be more deadly than its community counterpart. Hospital acquired pneumonia
occurs mostly in patients who are severely debilitated or who are immune suppressed.
Nosocomial pneumonia can generally be described as “early nosocomial” (appearing within five days of hospitalization) or “late nosocomial” (more than
five days after hospitalization). The nosocomial pneumonia of our patient was identified on the 3 rd day at the ICU which is also the 3rd day of his admission. The
organisms leading to community-acquired pneumonia, predominantly Gram-positive cocci, are seen in patients present with pneumonia very shortly after admission
to hospital (if no antibiotic therapy has so far been given) and Gram-negative bacilli predominate in patients developing pneumonia after five days of
hospitalization. The preliminary result of the tracheal aspirate revealed gram (-) woffi, acinetobacter hypersensitive to Ciprofloxacin and Piperacillin.
Symptoms
These may include fever, shortness of breath, and a cough that produces yellow, green, or gray sputum from the respiratory tract. Because nosocomial
pneumonia is such a serious infection, patients may need to receive more than one type of antibiotic to treat it. Getting pneumonia while in the hospital may prolong
the hospital stay, and intravenous (I.V.) antibiotic treatment usually lasts for up to 2 weeks. If patients begin to feel better, they may be switched from I.V. treatment
to oral (tablet) treatment. Patient had a productive cough with whitish sputum. Rales were heard on both lung fields.
Causes
Increased duration of hospital stay (risk increases with >14 days of stay).
•
Trauma (particularly head trauma).
•
Chronic underlying diseases (e.g. diabetes and chronic lung disease).
•
Immunosuppression.
•
General anaesthetic.
•
Endotracheal intubations. The patient was intubated for 12 days in the ICU, starting on his first day in the ICU
•
Hospital admission during the previous month.
•
Antibiotic history.
•
Diagnosis
• X-ray or CT scan.
5. Purulent sputum.
•
Fever.
•
Leucocytosis or leucopenia.
•
Laboratory Tests
• Blood cultures
• Sputum Gram stain and culture
The patient’s culture of sputum aspirate revealed gram (-) woffi, acinetobacter hypersensitive to Ciprofloxacin (C: Fluroquinolones; A: it inhibits bacterial cell
wall synthesis) and Piperacillin (C: Penicillin A: An extended-spectrum penicillin that inhibits cell-wall synthesis during microorganism multiplication.)
Treatment
Antibiotics used for hospital-acquired pneumonia include aminoglycosides, fluoroquinolones, carbapenems, and vancomycin.. Multiple antibiotics are
administered in combination in order to cover all the possible organisms effectively and rapidly, before the infectious agent can be known. The antibiotics
administered to the patient are the ff:. Ciprofloxacin 500mg 1 and ½ tab BID (C: Fluroquinolones; A: it inhibits bacterial cell wall synthesis); Clindamycin 300g 1
cup every 6 hrs (C: miscellaneous anti-infective; A: inhibits bacterial protein synthesis by binding to the 50S subunit of the ribosome) and Piperacillin +
Tazobactam 4.5 gm IVTT (C: Penicillin A: An extended-spectrum penicillin that inhibits cell-wall synthesis during microorganism multiplication. Tazobactam
increases piperacillin’s effectiveness by inactivating beta-lactamases, which destroy penicillins).
Management
Antibiotic treatment must be started promptly.
URINARY TRACT INFECTION
Definition
The second most common type of infection in the body. Women are especially prone to UTIs. One woman in five develops a UTI during her lifetime. UTIs
in men are not as common as in women but can be very serious when they do occur.
The urinary system consists of the kidneys, ureters, bladder, and urethra. The key elements in the system are the kidneys, a pair of purplish-brown organs located
below the ribs toward the middle of the back. The kidneys:
• remove excess liquid and wastes from the blood in the form of urine
• keep a stable balance of salts and other substances in the blood, and
• produce a hormone that aids the formation of red blood cells.
6. The narrow tubes called ureters, carry urine from the kidneys to the bladder, a sack-like organ in the lower abdomen. Urine is stored in the bladder and emptied
through the urethra
Urine is normally sterile -- thus, it does not normally contain bacteria. This is a good thing, since the mineral and sugar content of urine makes it a great medium for
bacteria to grow in. Several things keep bacteria out of the urine. These include:
· The urethral sphincter: when the urethra is squeezed shut, bacteria cannot climb up the urethra from the quot;meatusquot; (the outside opening) into the bladder.
· The length of the urethra: it's a long way up to the bladder for a bacterium. (A woman's urethra is shorter than a man's, which is one reason why women are
much more likely than men to get UTI's.)
· Frequent washing: any bacteria that make it into the urethra are flushed out the next time you urinate, and since most people empty their bladders almost
completely when they urinate any bacteria that get to the bladder will be flushed out too. There are also valves where the ureters enter the bladder to prevent
urine from quot;refluxingquot; from the bladder to the kidneys, so even if the bladder and its urine is infected the bacteria shouldn't travel up to the kidneys.
Symptoms
Not everyone with a UTI has symptoms, but most people get at least some symptoms. These may include a frequent urge to urinate and a painful, burning
feeling in the area of the bladder or urethra during urination. Often women feel an uncomfortable pressure above the pubic bone, and some men experience a
fullness in the rectum. It is common for a person with a urinary infection to complain that, despite the urge to urinate, only a small amount of urine is passed. The
urine itself may look milky or cloudy, even reddish if blood is present. A UTI does not normally cause fever if it is in the bladder or urethra. A fever may mean that
the infection has reached the kidneys. Other symptoms of a kidney infection include pain in the back or side below the ribs, nausea, or vomiting.
Cystitis may show up as burning on urination, often in the quot;middlequot; of urination. However, it may have no symptoms other than fever, lower
abdominal (just above the pubic bone) pain, or even just a funny smell or colour or appearance (cloudy, dark, even blood-tinged) to your urine. And since kidneys
are located at back, just below the bottom ribs, pyelonephritis may appear as pain at the back or flank(s), or in the abdomen. Fever usually (but not always) comes
along with the pain. If the kidneys are severely affected, one may also start seeing some of the complications due to kidney malfunction.
Complications
The biggest problem with a UTI is if it progresses to pyelonephritis. This can result in scarring and damage to the kidney tissue. If there is enough damage to
the filter system, waste products can't be removed properly. This constitutes kidney failure, and if it is bad enough and long-lasting enough, the only solutions are
dialysis (filtering blood through an quot;artificial kidneyquot;) or a kidney transplant
A different complication occurs if the pressure-regulation tissues in the kidney are scarred. If this is bad enough, your blood pressure may be kept too low
(and one may faint frequently at the very least) or too high (leading to strokes, heart disease).
Causes
7. Since urine is normally sterile. It is usually free of bacteria, viruses, and fungi but does contain fluids, salts, and waste products. An infection occurs when
tiny organisms, usually bacteria from the digestive tract, cling to the opening of the urethra and begin to multiply. The urethra is the tube that carries urine from the
bladder to outside the body. Most infections arise from one type of bacteria, Escherichia coli (E. coli), which normally lives in the colon. In many cases, bacteria
first travel to the urethra. When bacteria multiply, an infection can occur.
• An infection limited to the urethra is called Urethritis.
This can be due to other things besides the organisms usually involved in UTI's; in particular, many sexually-transmitted diseases (STD's) appear initially as
urethritis. Another is stool-related bacteria (the most common bacteria on the skin near the meatus) will also often cause urethritis.
• If bacteria move to the bladder and multiply, a bladder infection, called Cystitis, results.
This is the most common form of UTI; it can be aggravated if the bladder does not empty completely when urinating.
• An infection of the ureter is called, Ureteritis. This can occur if the bacteria entered the urinary tract from above, or if the ureter-to-bladder valves don't work
properly and allow urine to quot;refluxquot; from the bladder into the ureters.
• If the infection is not treated promptly, bacteria may then travel further up the ureters to multiply and infect the kidneys. A kidney infection is called
Pyelonephritis.
Microorganisms called Chlamydia and Mycoplasma may also cause UTIs in both men and women, but these infections tend to remain limited to the urethra
and reproductive system. Unlike E. coli, Chlamydia and Mycoplasma may be sexually transmitted, and infections require treatment of both partners.
The urinary system is structured in a way that helps ward off infection. The ureters and bladder normally prevent urine from backing up toward the kidneys,
and the flow of urine from the bladder helps wash bacteria out of the body. In men, the prostate gland produces secretions that slow bacterial growth. In both sexes,
immune defenses also prevent infection. But despite these safeguards, infections still occur.
Risk Factors
Any abnormality of the urinary tract that obstructs the flow of urine (a kidney stone, for example) sets the stage for an infection. An enlarged prostate gland
also can slow the flow of urine, thus raising the risk of infection.
A common source of infection is catheters, or tubes, placed in the urethra and bladder. The patient has been catheterized since December 5, 2006 until
December 12, 2006 (7 days), was inserted on December 14, 2006. Urinary Tract infection was diagnosed on December 26, 2006. So on December 27, 2006 FBC
was removed. A person who cannot void or who is unconscious or critically ill often needs a catheter that stays in place for a long time. Some people, especially the
8. elderly or those with nervous system disorders who lose bladder control, may need a catheter for life. Bacteria on the catheter can infect the bladder, thus, hospital
staff take special care to keep the catheter clean and remove it as soon as possible.
People with diabetes have a higher risk of a UTI because of changes in the immune system. Any other disorder that suppresses the immune system raises the
risk of a urinary infection.
Diagnosis
A sample of urine is tested for pus and bacteria. A quot;clean catchquot; urine sample is collected by washing the genital area and collecting a quot;midstreamquot; sample of
urine in a sterile container.
In the urinalysis test, the urine is examined for white and red blood cells and bacteria. Bacteria are then grown in a culture and tested against different
antibiotics to see which drug best destroys the bacteria. This last step is called a sensitivity test. Some microbes, like Chlamydia and Mycoplasma, can be detected
only with special bacterial cultures. A doctor suspects one of these infections when a person has symptoms of a UTI and pus in the urine, but a standard culture fails
to grow any bacteria.
The results of the patients urinalysis, revealed cloudy appearance, RBC of 5-10/hpf, epithelial cells of 2-5/hpf, moderate(++) blood, 30(++)protein and heat
& acetic acid: (+)
An ultrasound exam is also used, which gives pictures from the echo patterns of soundwaves bounced back from internal organs. Another useful test is
cystoscopy. A cystoscope is an instrument made of a hollow tube with several lenses and a light source, which allows the doctor to see inside the bladder from the
urethra.
Treatment
UTIs are treated with antibacterial drugs. The choice of drug and length of treatment depend on the patient's history and the urine tests that identify the
offending bacteria. The sensitivity test is especially useful in helping the doctor select the most effective drug. A class of drugs called quinolones includes four
drugs approved in recent years for treating UTI. These drugs include ofloxacin (Floxin), norfloxacin (Noroxin), ciprofloxacin (Cipro), and trovafloxin (Trovan). A
followup urinalysis helps to confirm that the urinary tract is infection-free. It is important to take the full course of treatment because symptoms may disappear
before the infection is fully cleared.
Various drugs are available to relieve the pain of a UTI. A heating pad may also help. Most doctors suggest that drinking plenty of water helps cleanse the
urinary tract of bacteria. During treatment, it is best to avoid coffee, alcohol, and spicy foods. And one of the best things a smoker can do for his or her bladder is to
quit smoking. Smoking is the major known cause of bladder cancer.
9. Management
• Drink plenty of water every day.
• Urinate when you feel the need; don't resist the urge to urinate.
• Wipe from front to back to prevent bacteria around the anus from entering the vagina or urethra.
• Take showers instead of tub baths.
• Cleanse the genital area before sexual intercourse.
In women, avoid using feminine hygiene sprays and scented douches, which may irritate the urethra.
Anatomy & Physiology
Brain
Major regions of the brain and their functions
10. The major regions of the brain are the cerebral hemispheres, diencephalon, brain stem and cerebellum.
Cerebral hemispheres
The cerebral hemispheres, located on the most superior part of the brain, are separated by the longitudinal fissure. They make up approximately 83% of total brain
mass, and are collectively referred to as the cerebrum. The cerebral cortex constitutes a 2-4 mm thick grey matter surface layer and, because of its many
convolutions, accounts for about 40% of total brain mass. It is responsible for conscious behaviour and contains three different functional areas: the motor areas,
sensory areas and association areas. Located internally are the white matter, responsible for communication between cerebral areas and between the cerebral cortex
and lower regions of the CNS, as well as the basal nuclei (or basal ganglia), involved in controlling muscular movement.
Midbrain
Function: Controls Responses to Sight, Eye Movement, Pupil Dilation, Body Movemen,t Hearing.
Location: The mesencephalon/midbrain is the most rostral portion of the brainstem. It is located between the forebrain and brainstem.
Forebrain
Function: Chewing ,Directs Sense Impulses Throughout the Body ,Equilibrium ,Eye Movement, Vision ,Facial Sensation Hearing, Phonation ,Intelligence Memory,
Personality Respiration
Salivation, Swallowing Smell, Taste
Location: The prosencephalon/forbreain is the most anterior portion of the brain.
Diencephalon
The diencephalon is located centrally within the forebrain. It consists of the thalamus, hypothalamus and epithalamus, which together enclose the third ventricle.
The thalamus
acts as a grouping and relay station for sensory inputs ascending to the sensory cortex and association areas. It also mediates motor activities, cortical arousal and
memories. The
hypothalamus, by controlling the autonomic (involuntary) nervous system, is responsible for maintaining the body’s homeostatic balance. Moreover it forms a part
of the limbic
system, the ‘emotional’ brain. The epithalamus consists of the pineal gland and the CSF producing choroid plexus.
Brain stem
The brain stem is similarly structured as the spinal cord: it consists of grey matter surrounded by white matter fibre tracts. Its major regions are the midbrain, pons
and medulla oblongata. The midbrain, which surrounds the cerebral aqueduct, provides fibre pathways between higher and lower brain centres, contains visual and
auditory reflex and subcortical motor centres. The pons is mainly a conduction region, but its nuclei also contribute to the regulation of respiration and cranial
nerves. The medulla oblongata takes an important role as an autonomic reflex centre involved in maintaining body homeostasis. In particular, nuclei in the medulla
11. regulate respiratory rhythm, heart rate, blood pressure and several cranial nerves. Moreover, it provides conduction pathways between the inferior spinal cord and
higher brain centres.
Cerebral Cortex Lobes
Frontal Lobe
Function: Motor Functions Higher Order Functions Planning Reasoning Judgement Impulse Control Memory
Location: The frontal lobes are the anterior portion of the cerebral cortex.
Occipital Lobe
Function: Controls Vision Color Recognition
Location: The occipital lobes are the most caudal portion of the cerebral cortex.
Parietal Lobe
Function: Cognition Information Processing Pain and Touch Sensation Spatial Orientation Speech Visual Perception
Location: The parietal lobes are anterior to the occipital lobes and posterior to the central sulcus (fissure) and frontal lobes.
Temporal Lobe
Function: Emotional Responses Hearing Memory Speech
Location: The temporal lobes are anterior to the occipital lobes and lateral to the Fissure of Sylvius.
Insula
Function: Associated With Visceral Functions Integrates Autonomic Information
Location: The insula is located within the cerebral cortex, beneath the frontal, parietal and temporal opercula.
Cerebellum
The cerebellum, which is located dorsal to the pons and medulla, accounts for about 11% of total brain mass. Like the cerebrum, it has a thin outer cortex of grey
matter, internal white matter, and small, deeply situated, paired masses (nuclei) of grey matter. The cerebellum processes impulses received from the cerebral motor
cortex, various brain stem nuclei and sensory receptors in order to appropriately control skeletal muscle contraction, thus giving smooth, coordinated movements.
The cerebral circulatory system
Blood is transported through the body via a continuous system of blood vessels. Arteries carry oxygenated blood away from the heart into capillaries supplying
tissue cells. Veins collect the blood from the capillary bed and carry it back to the heart. The main purpose of blood flow through body tissues is to deliver oxygen
and nutrients to and waste from the cells, exchange gas in the lungs, absorb nutrients from the digestive tract, and help forming urine in the kidneys. All the
circulation besides the heart and the pulmonary circulation is called the systemic circulation.
12. The internal carotid arteries, branches of the common carotid arteries, run through the neck and enter the skull through the temporal bone. Once inside the
cranium, each divides into the anterior and middle cerebral arteries, which supply most of the cerebrum.
The paired vertebral arteries pass upward from the subclavian arteries at the base of the neck. Within the skull, the vertebral arteries join to form the single
basilar artery, which serves the brain stem and cerebellum as it travels upward. At the base of the cerebrum, the basilar artery divides to form the posterior cerebral
arteries, which supply the posterior part of the cerebrum.
The anterior and posterior blood supplies of the brain are united by small communicating arterial branches. The result is a complete circle of connecting
blood vessels called the circle of Willis, which surrounds the base of the brain. The circle of Willis protects the brain, because it provides more than one route for
blood to reach brain tissue in case of a clot or impaired blood flow anywhere in the system.
Respiratory System
13. The respiratory system is composed of the nose, the pharynx, the larynx, the trachea, the bronchi & their smaller branches and the lungs. The major function
of this system is to supply the body with oxygen and dispose carbon dioxide from the body.
During breathing, air enters the body through the nose which is the only externally visible part of the respiratory system. The air passes through the external
nares then to the nasal cavity where it is first filtered and warmed. After which passes through pharynx or most commonly known as the “throat” which is the
common passageway for both food and air. After passing through the pharynx, the air is now being routed to its proper channel by the larynx also known as the
“voice box” which is lies just below the pharynx. The epiglottis protects the superior opening of the larynx which closes as the person swallows so that food will not
enter into the trachea, also called the “windpipe”. The trachea extends from the larynx to the primary bronchi. As the air comes down the trachea and enters the
right and left primary bronchi, it is again filtered by the ciliated mucosa lining which propels dust particles and other debris away from the lungs. From the
subdivision of the trachea results the left and right primary bronchi which are the ones plunged into the hilus of the lungs on its sides. By the time air reaches the
bronchi, it is already warm, cleansed and well humidified but because the right primary bronchi is wider, shorter and straighter than the left, inhaled foreign objects
are consequently lodged in it. After the primary bronchi enter the lungs, they subdivide into smaller and smaller branches called bronchioles, until it
terminates/ends in clusters of alveoli (air sacs) inside the lungs where gas exchange takes place.
14. The paired lungs are fairly large organs. They occupy the entire thoracic cavity except for the most central area, the mediastinum, which houses the heart,
the great blood vessels, bronchi, esophagus, and other organs. The narrow superior portion of each lung, the apex, is located just deep to the clavicle. The broad
lung area resting on the diaphragm is the base. Each lung is divided into lobes by fissures; the left lung has two lobes, and the right lung has three.
The surface of each lung is covered with a visceral serosa called the pulmonary, or visceral, pleura and the walls of the thoracic cavity are lined by the
parietal pleura. The pleural membranes produce pleural fluid, a slippery serous secretion which allows the lungs to glide easily over the thorax wall during
breathing movements and causes the two pleural layers to cling together. The pleurae can slide easily from side to side across one another, but they strongly resist
being pulled apart. Consequently, the lungs are held tightly to the thorax wall, and the pleural space is more of a potential space than an actual one. As described
shortly, this condition of tightly adhering pleural membranes is absolutely essential for normal breathing.
After the primary bronchi enter the lungs, they subdivide into smaller and smaller branches (secondary and tertiary bronchi, and so on), finally ending in the
smallest of the conducting passageways, the bronchioles. Because of this branching and rebranching of the respiratory passageways within the lungs, the network
formed is often referred to as the bronchial or respiratory tree. All but the smallest branches have reinforcing cartilage in their walls.
The terminal bronchioles lead into respiratory zone structures, even smaller conditions that eventually terminate in alveoli, or air sacs. The respiratory zone,
which includes the respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli, is the only site of gas exchange. All other respiratory passages are conducting
zone structures that serve as conduits to and from the respiratory zone. There are millions of the clustered alveoli, which resemble bunches of grapes, and they
make up the bulk of the lungs. The balance of the lung tissue, its stroma, is elastic connective tissue. Thus, in spite of their relatively large size, the lungs weigh only
about 2 ½ pounds, and they are soft and spongy.
The Respiratory Membrane
The walls of the alveoli are composed largely of a single, thin layer of squamous epithelial cells. The thinness of their walls is hard to imagine, but a sheet of
tissue paper is much thicker. Alveolar pores connect neighboring air sacs and provide alternate routes for air to reach alveoli whose feeder bronchioles have been
clogged by mucus or otherwise blocked. The external surfaces of the alveoli are covered with a “cobweb” of pulmonary capillaries. Together, the alveolar and
capillary walls and their fused basement membranes construct the respiratory membrane (air-blood barrier), which has gas (air) flowing past on one side and
blood flowing past on the other. The gas exchanges occur by simple diffusion through the respiratory membrane – oxygen passing from the alveolar air into the
capillary blood and carbon dioxide leaving the blood to enter the gas-filled alveolus. It has been estimated that the total gas exchange surface provided by the
alveolar walls of a healthy man is 50 to 70 square meters, or approximately 50 times greater than the surface area of the skin. The final line of defense for the
respiratory system is in the alveoli. Macropahges, sometimes called “dust cells,” wander in and out of the alveoli picking up bacteria, carbon particles, and other
debris. Also scattered amid the epithelial cells that form most of the alveolar walls are chunky cuboidal cells, which look very different. The cuboidal cells produce
a lipid (fat) molecule called surfactant, which coats the gas-exposed alveolar surfaces and is very important in lung function.
15. Urinary System
The urinary system consists of the kidneys, ureters, urinary bladder, and urethra. The kidneys form the urine and account for the other functions attributed to the
urinary system. The ureters carry the urine away from kidneys to the urinary bladder, which is a temporary reservoir for the urine. The urethra is a tubular structure
that carries the urine from the urinary bladder to the outside.
Kidneys
The kidneys are the primary organs of the urinary system. The kidneys are the organs that filter the blood, remove the wastes, and excrete the wastes in the urine.
They are the organs that perform the functions of the urinary system. The other components are accessory structures to eliminate the urine from the body.
The paired kidneys are located between the twelfth thoracic and third lumbar vertebrae, one on each side of the vertebral column. The right kidney usually is slightly
lower than the left because the liver displaces it downward. The kidneys protected by the lower ribs, lie in shallow depressions against the posterior abdominal wall
and behind the parietal peritoneum. This means they are retroperitoneal. Each kidney is held in place by connective tissue, called renal fascia, and is surrounded by a
16. thick layer of adipose tissue, called perirenal fat, which helps to protect it. A tough, fibrous, connective tissue renal capsule closely envelopes each kidney and
provides support for the soft tissue that is inside.
In the adult, each kidney is approximately 3 cm thick, 6 cm wide, and 12 cm long. It is roughly bean-shaped with an indentation, called the hilum, on the medial
side. The hilum leads to a large cavity, called the renal sinus, within the kidney. The ureter and renal vein leave the kidney, and the renal artery enters the kidney at
the hilum.
The outer, reddish region, next to the capsule, is the renal cortex. This surrounds a darker reddish-brown region called the renal medulla. The renal medulla consists
of a series of renal pyramids, which appear striated because they contain straight tubular structures and blood vessels. The wide bases of the pyramids are adjacent
to the cortex and the pointed ends, called renal papillae, are directed toward the center of the kidney. Portions of the renal cortex extend into the spaces between
adjacent pyramids to form renal columns. The cortex and medulla make up the parenchyma, or functional tissue, of the kidney.
The central region of the kidney contains the renal pelvis, which is located in the renal sinus and is continuous with the ureter. The renal pelvis is a large cavity that
collects the urine as it is produced. The periphery of the renal pelvis is interrupted by cuplike projections called calyces. A minor calyx surrounds the renal papillae
of each pyramid and collects urine from that pyramid. Several minor calyces converge to form a major calyx. From the major calyces the urine flows into the renal
pelvis and from there into the ureter.
Each kidney contains over a million functional units, called nephrons, in the parenchyma (cortex and medulla). A nephron has two parts: a renal corpuscle and a
renal tubule.The renal corpuscle consists of a cluster of capillaries, called the glomerulus, surrounded by a double-layered epithelial cup, called the glomerular
capsule. An afferent arteriole leads into the renal corpuscle and an efferent arteriole leaves the renal corpuscle. Urine passes from the nephrons into collecting ducts
then into the minor calyces.
The juxtaglomerular apparatus, which monitors blood pressure and secretes renin, is formed from modified cells in the afferent arteriole and the ascending limb of
the nephron loop.
Ureters
Each ureter is a small tube, about 25 cm long, that carries urine from the renal pelvis to the urinary bladder. It descends from the renal pelvis, along the posterior
abdominal wall, behind the parietal peritoneum, and enters the urinary bladder on the posterior inferior surface.
The wall of the ureter consists of three layers. The outer layer, the fibrous coat, is a supporting layer of fibrous connective tissue. The middle layer, the muscular
coat, consists of inner circular and outer longitudinal smooth muscle. The main function of this layer is peristalsis to propel the urine. The inner layer, the mucosa, is
transitional epithelium that is continuous with the lining of the renal
17. pelvis and the urinary bladder. This layer secretes mucus which coats and protects the surface of the cells.
Urinary Bladder
The urinary bladder is a temporary storage reservoir for urine. It is located in the pelvic cavity, posterior to the symphysis pubis, and below the parietal peritoneum.
The size and shape of the urinary bladder varies with the amount of urine it contains and with pressure it receives from surrounding organs.
The inner lining of the urinary bladder is a mucous membrane of transitional epithelium that is continuous with that in the ureters. When the bladder is empty, the
mucosa has numerous folds called rugae. The rugae and transitional epithelium allow the bladder to expand as it fills.
The second layer in the walls is the submucosa that supports the mucous membrane. It is composed of connective tissue with elastic fibers.
The next layer is the muscularis, which is composed of smooth muscle. The smooth muscle fibers are interwoven in all directions and collectively these are called
the detrusor muscle. Contraction of this muscle expels urine from the bladder. On the superior surface, the outer layer of the bladder wall is parietal peritoneum. In
all other regions, the outer layer is fibrous connective tissue.
There is a triangular area, called the trigone, formed by three openings in the floor of the urinary bladder. Two of the openings are from the ureters and form the
base of the trigone. Small flaps of mucosa cover these openings and act as valves that allow urine to enter the bladder but prevent it from backing up from the
bladder into the ureters. The third opening, at the apex of the trigone, is the opening into the urethra. A band of the detrusor muscle encircles this opening to form
the internal urethral sphincter.
Urethra
The final passageway for the flow of urine is the urethra, a thin-walled tube that conveys urine from the floor of the urinary bladder to the outside. The opening to
the outside is the external urethral orifice. The mucosal lining of the urethra is transitional epithelium. The wall also contains smooth muscle fibers and is supported
by connective tissue.
The internal urethral sphincter surrounds the beginning of the urethra, where it leaves the urinary bladder. This sphincter is smooth (involuntary) muscle. Another
sphincter, the external urethral sphincter, is skeletal (voluntary) muscle and encircles the urethra where it goes through the pelvic floor. These two sphincters control
the flow of urine through the urethra.
In females, the urethra is short, only 3 to 4 cm (about 1.5 inches) long. The external urethral orifice opens to the outside just anterior to the opening for the vagina.
18. In males, the urethra is much longer, about 20 cm (7 to 8 inches) in length, and transports both urine and semen. The first part, next to the urinary bladder, passes
through the prostate gland and is called the prostatic urethra. The second part, a short region that penetrates the pelvic floor and enters the penis, is called the
membranous urethra. The third part, the spongy urethra, is the longest region. This portion of the urethra extends the entire length of the penis, and the external
urethral orifice opens to the outside at the tip of the penis.
CLIENT IN CONTEXT PRESENT STATE INTERVENTIONS EVALUATION
PHYSICAL EXAMINATION:
Informant: father and eldest son,
Date: December 13, 2006, 1:45
mostly father
pm, Wednesday
65% Reliability
G.M., 37 y.o., male, married, General appearance:
Roman Catholic, Filipino, Seen lying on bed, awake,
currently residing in Tisa conscious, responsive to pain,
19. afebrile, with O2 inhalation @ 2L/
Labangon, Cebu city, was
minute via nasal cannula, with
admitted for the first time in
NGT @ left nostril, with FBC
CVGH on November 24, 2006 at
draining well to CDU, with the
7:00pm via taxi accompanied by
following v/s: BP: 130/90 mmHg,
co-worker for complaint of
PR: 62 bpm, RR: 15 cpm, T:
weakness on the lower extremities
36.5°C/ axilla, height: 5’6” IBW =
noted 5 hours PTA, under the
service of Dr. Pama of the
SKIN:
Department of Family Medicine
warm, dry, good skin tugor, with
and co-managed by Dr. Español of
scalings found on both lower
the Department of Internal
extremities, no rashes, dark
Medicine with the case # 84334.
complexion, a grade 2 bed sore
History of present illness: located approx. 1/2 inch in
5 days , patient had history diameter, circular in form at the
of profuse diarrhea approximately inner leg of the left ankle and
10-15 episodes per day amounting approx. 2 inches in diameter,
to 1cup per episode. No meds irregular in form 1 inch above the
taken nor hydration correction outer right ankle
done. Condition tolerated. NAIL:
Few hours PTA, patient had pinkish nail bed, smooth and short,
weakness of the lower extremities dirty fingernails, CRT <2 seconds,
no clubbing of nails
associated with numbness which
HAIR & HEAD:
progressively reached the level
evenly distributed short, black
below the umbilicus. Patient was
hair, no lesions, no lice
unable to stand alone, prompting
infestations, no dandruff, hair is
to seek consult at CVGH-(Cebu
smooth, normocephalic
Velez General Hospital) and
subsequently admitted. Labs taken EYES:
outer canthus of eye is inline with
were potassium which showed
the pinna, eyebrows and eyelashes
hypokalemia at 1.5mmOl/L and
mild QRS complexes documented evenly distributed, no discharges,
on ECG. Pt. was the transferred to pinkish palpebral conjunctivae, iris
20. and pupil are round in shape,
ICU for further monitoring. ABG
sclera is white, eyes are
was likewise taken because he
symmetrical in shape, (+)
complained of dyspnea which
PERRLA,(-) cardinal gaze, (-)
revealed acidosis with adequate
peripheral gaze, cannot see
oxygenation.
EARS:
On first day at ICU, pt. pinna is in line with the outer
complained of persistent dyspnea. canthus of the eye, symmetrical,
Pulse oximetry revealed 98-100%. no tenderness, no abnormal or foul
Approval of the family was done discharges, can hear spoken words
pertaining of possible intubation if at 1 ft. distance
respiratory arrest would occur 30 NOSE:
mins later. O2 saturated declined With NGT @ left nostril, nasal
to less than 90% and was septum at midline, no discharges,
subsequently intubated with patent airway, sinuses not tender,
continuous ambubagging at (+) frontal and maxillary
10L/min. Along the course of transillumination
intubation, pt went into MOUTH:
cardiopulmonary arrest and was pinkish and moist lips, pink
resuscitated accordingly. mucosa, no lesions, tongue at the
floor of the mouth, 30 teeth,
On the second day, CBC was
NECK:
taken which showed WBC of 10.4
supple, located at midline, no
k/uL(4.10-10.9 k/uL) and serum
tenderness, no lymphadenopathy,
potassium of 2.1 mmOl/L(3.5-
trachea located at midline, no
5mmOl/L). Pt was comatosed with
masses or lesions noted
blank stare. Citicoline 1 gm IVTT
CHEST and LUNGS:
(C: CNS stimulant; A: it produces
Presence of tattoo located @ the
CNS stimulation by increasing
right scapular region, no palpable
level of neurotransmitters in the
lesions, no bruises, no masses
CNS. Produce CNS stimulation
palpated, equal chest expansion,
and respiratory stimulation dilated
rales on both lung fields
pupils, increase motor activity and
CARDIOVASCULAR:
mental alertness, and a diminished
21. no murmurs heard, distinct S1 &
sense of fatigue.); Esomeprazole
S2, regular rhythm, PR:62 bpm
40mg IVTT OD (C: Anti-ulcer,
ABDOMEN:
proton pump inhibitor; A: binds an
protuberant, umbilicus at midline,
enzyme on gastric parietal cells in
5 clicks/min. no masses palpated,
the presence of acidic gastric pH,
no abdominal distention
preventing the final transport of
GENITALIA:
hydrogen ion into the gastric
grossly male, no discharges, no
lumen); kalium durule, 2 durules
lesions noted
QID (C: mineral and electrolyte
EXTREMITIES:
replacement or supplement; A:
upper extremities and lower
replaces potassium and maintains
extremities are symmetrical in size
potassium level); sodium
and in decorticate state, palpable
bicarbonate gr10 1 tab TID (C:
peripheral pulses, a grade 2 bed
alkalinizer; A: restores buffering
sore located approx. 1/2 inch in
capacity of the body and
diameter, circular in form at the
neutralizes excess acid) were
inner leg of the left ankle and
likewise given.
approx. 2 inches in diameter,
On the third day at ICU, irregular in form 1 inch above the
preliminary result of the tracheal outer right ankle
aspirate revealed acinetobacter
woffi sensitive to ciprofloxacin Neurologic assessment:
and Piperacillin + Tazobactam. MENTAL STATUS: conscious,
Thus was started on Ciprofloxacin incoherent, with GCS of 6
500mg 1 and ½ tab BID (C: SENSORY STATUS: cannot be
Fluroquinolones; A: it inhibits assessed
bacterial cell wall synthesis); MOTOR STATUS: cannot be
Clindamycin 300g 1 cup every 6 assessed
hrs (C: miscellaneous anti-
infective; A: inhibits bacterial CRANIAL NERVES:
protein synthesis by binding to the I: n/a
50S subunit of the ribosome) and II: n/a
Piperacillin + Tazobactam 4.5 gm III, IV, VI: (+) PERRLA, (-)
IVTT (C: Penicillin A: An
22. cardinal gaze, (-) peripheral gaze
extended-spectrum penicillin that
V: (+) blink reflex, can open &
inhibits cell-wall synthesis during
close mouth,
microorganism multiplication.
VII: n/a
Tazobactam increases
VIII: can hear spoken words at 1
piperacillin’s effectiveness by
ft. distance
inactivating beta-lactamases,
IX, X: n/a
which destroy penicillins).
XI: n/a
Potassium was taken with a result
XII: (+) gag reflex
of 3.7 mmol/L.
On the 12th day of ICU, pt DEEP TENDON REFLEXES:
was extubated but weaning with T- Biceps: (+), triceps (+)
piece at 4 LPM was done a day
before which he tolerated. Then MUSCLE STRENGTH:
nebulization with Salbutamol 1/5 1/5
and Hydrocortisone was done. 1/5 1/5
Finally he was transferred to Ward Date: December 18, 2006, 10:15
though still comatose with blank am Monday
stare. He had a working diagnosis
of 1 Hypoxic – Ischemic General appearance:
Encephalopathy 2 severe Seen lying on bed, awake,
hypokalemia - corrected 3 conscious, incoherent, afebrile,
Nosocomial pneumonia with NGT @ left nostril, with O2
inhalation @ 2L/minute via nasal
Past history illness:
cannula, with FBC draining well
Patient is known
to CDU, with the following v/s:
hypertensive with unrecalled bp,
BP: 120/80 mmHg, PR: 69 bpm,
non-diabetic, non-asthmatic with
RR: 22 cpm, T: 36.7°C/ axilla,
no known food and drug allergies.
He is a non-smoker and an
SIGNIFICANT FINDINGS:
occasional alcoholic beverage
drinker. Heredofamilial disease
•
includes hypertension on maternal (-) cardinal and
side and cancer on the paternal (-)peripheral gaze
23. • still can’t see
side.
• with O2 inhalation @
Previous hospitalization:
2L/min
1st hospitalization was in the
• with NGT @ left nostril
1990s due to appendectomy.
• presence of tattoo at right
However patient’s father forgot
scapular region
the details pertaining to it such as
• rales in both lung fields
the name of the hospital, doctor,
• dirty fingernails
and take home meds.
• with FBC draining well to
2nd hospitalization was in
CDU
1993 at unrecalled hospital with
• Both upper and lower
the diagnosis of urolithiasis.
extremities are still in
Surgery was done. Number of
decorticate state
days in the hospital and take home
• a grade 2 bed sore located
meds were unrecalled. Patient’s
approx. 1/2 inch in
condition improved upon
diameter, circular in form
discharged.
at the inner leg of the left
1. Health perception - Health ankle and approx. 2 inches
management Pattern in diameter, irregular in
When he was still residing form 1 inch above the
at Manila, he had a regular check outer right ankle
up at Genreal hospital, Pasig City • with scalings found both
under Dr. Casino. Now that he is on lower extremities
residing in Cebu for three years, Date: December 19, 2006, 10: 15
S.O. doesn’t know if the patient am Tuesday
still practices regular check-ups.
Patient takes OTC drugs. If he has General appearance:
fever, he takes Biogesic (C: Seen lying on bed, awake,
antipyretic and anti-inflammatory conscious, incoherent, afebrile,
A: Inhibits the synthesis of with O2 inhalation @ 2L/minute
prostaglandin that serve as via nasal cannula, with NGT @
mediators of pain and fever left nostril, with FBC draining
primarily in the CNS) and if he has well to CDU, with the following v/
24. s: BP: 130/90 mmHg, PR: 79 bpm,
colds, he takes Neozep and
RR: 20 cpm, T: 365°C/ axilla,
afforded relief. He does not take
herbal medicines and does not
SIGNIFICANT FINDINGS:
believe in folk healers. S.O.
doesn’t know if patient performs
• (-) cardinal and
TSE. Patient is fully immunized,
(-)peripheral gaze
and goes to the dentist when need
• still can’t see
arises.
• with O2 inhalation @
2. Nutritional-metabolic Pattern
2L/min
Patient eats 3 to 4 times a
• with NGT @ left nostril
day with snacks in the morning,
• presence of tattoo at right
afternoon and evening. He usually
scapular region
eats breakfast at 7 to 8 am
• rales in both lung fields
comprising of egg, rice and milo.
• with FBC draining well to
If rice is unavailable, he replaces
CDU
them with bread. He takes his
• Both upper and lower
lunch at 12 to 1 pm and usually
extremities are still in
eats fried meat, at least 3cups of
decorticate state
rice and cold water. Dinner is
•
taken at around 7 – 8 pm a grade 2 bed sore located
comprising of meat, at least 3 cups approx. 1/2 inch in
of rice and cold water. Patient's diameter, circular in form
favorite food is adobong baboy at the inner leg of the left
and prefers to drink cold water. He ankle and approx. 2 inches
does not have intolerance to any in diameter, irregular in
type of food and can chew and form 1 inch above the
swallow without difficulty. He outer right ankle
does not take any vitamins and • with scalings found both
supplements. The last time he took on lower extremities
multivitamins is when he was 7
years old brand name unrecalled. Date: December 20, 2006 1:45 pm,
Patient drinks at least 8 glasses of Wednesday
water/day.
25. General appearance:
During hospitalization, Px is
Seen lying on bed, awake
currently on NGT since he was
conscious, inoherent, afebrile, with
released at ICU at Dec 5, 2006.
O2 inhalation @ 2L/minute via
His diet prescription is 1800cal in
nasal cannula, with NGT @ left
1000cc volume into 6 equal
nostril, with FBC draining well to
feedings with 300cc as
CDU, with the following v/s: BP:
volume/feeding. On December 18,
120/90 mmHg, PR: 66 bpm, RR:
2006 his diet prescription was
24 cpm, T: 36.6 °C/axilla
increased to 2500 cal in 2500 cc
volume with the same
SIGNIFICANT FINDINGS:
specification and 100 cc water
every 4 hours per NGT.
• (-) cardinal and
3. Elimination pattern Pattern (-)peripheral gaze
S.O. doesn’t know patient’s
• still can’t see
elimination pattern before
• with O2 inhalation @
admission but claimed that the px
2L/min
does not use any laxatives. When
• with NGT @ left nostril
patient experiences constipation,
• presence of tattoo at right
he just drinks lots of water and
scapular region
when experiences diarrhea, patient
• rales in both lung fields
takes in Lomotil or Diatabs
• with FBC draining well to
During hospitalization,
CDU
Patient is currently w/ Foley bag
• Both upper and lower
catheter draining well to clsed
extremities are still in
drainage unit (Fbc-cdu) since
decorticate state
released on December 5, 2006 and
• a grade 2 bed sore located
urinates more than 1,000ml of
approx. 1/2 inch in
urine per day with a dark yellow
diameter, circular in form
colored urine. On December 12,
at the inner leg of the left
2006 FBC was removed but
ankle and approx. 2 inches
patient experienced bladder
in diameter, irregular in
distention, which was then
form 1 inch above the
26. outer right ankle
relieved by hot and cold compress
• with scalings found both
but due to persistent bladder
on lower extremities
distention FBC, was inserted on
December 14, 2006. Urinary Tract
Date: January 3, 2007 9:30 am
infection was diagnosed on
Wednesday
December 26, 2006. So on
December 27, 2006 FBC was
General appearance:
removed and was not reinserted
Seen lying on bed, asleep, afebrile,
again because patient was able to
with NGT @ left nostril, with the
void thereafter and also due to the
following v/s: BP: 120/80 mmHg,
UTI. He defecates everyday with a
PR: 89 bpm, RR: 20 cpm, T:
yellow watery stool. Patient
36.5°C/ axilla,
experiences urinary and bowel
incontinence and constantly wears
SIGNIFICANT FINDINGS:
diaper up to present.
• (-) cardinal and
4. Activity-exercise pattern
(-)peripheral gaze
Patient is a supervisor at
• still can’t see
global insurance for 3 yrs. S.O.
• with NGT @ left nostril
does not know his daily activities,
• presence of tattoo at right
and time of patient's work and
scapular region
patient does not engage in any
• rales in both lung fields
form of exercise and sports.
• Both upper and lower
Patient used to play basketball
extremities are still in
with friends at least once a week
decorticate state
but stopped after he got married.
• with scalings found both
Patient’s form of recreation
on lower extremities
include reading, sleeping, and
• A whitish, grade 2
watching tv.
bedsore, half inch in
During hospitalization,
diameter, circular in form
patient is always on hospital bed
was noted on the left inner
and cannot change positions such
ankle and a reddish, grade
as turning to sides, sitting down
2 bedsore, one inch in
27. diameter, irregular in form
and standing up on his own. He
was noted 1 inch above the
has a schedule positioning every 2
right outer ankle
hours. He depends on his S.O. in
doing his ADL’s.
5. Sleep-rest pattern Date: January 8, 2007 10:30 am
When patient is on a Monday
vacation in Manila, S.O. said that
the patient usually sleeps at around General appearance:
9pm shortly after eating snacks Seen lying on bed, asleep, with
and wakes up at around 9am. And NGT left nostril, with the
he does not take any sleeping following v/s: BP 110/80 mmHg,
medications. Patient takes nap for PR: 79 bpm, RR: 18 cpm, T:
about 1-3 hours in the afternoon. 36.4°C/axilla
Patient prefers to sleep in a cold
room and uses 2 pillows. S.O. does SIGNIFICANT FINDINGS:
not know if the patient experiences
nightmares. • (-) cardinal and
During hospitalization, (-)peripheral gaze
•
patient sleeps most of the time. still can’t see
• with NGT @ left nostril
6. Cognitive-perceptual pattern
• presence of tattoo at right
Patient does not wear
scapular region
eyeglasses and does not have any
• rales in both lung fields
hearing problems. Patient is a
•
college graduate with a course of distended bladder
banking finance. S.O. couldn’t • Both upper and lower
recall the name of the school. extremities are still in
decorticate state
• A whitish, grade 2
7. Role-relationship pattern
bedsore, half inch in
The patient, as described
diameter, circular in form
by his father is a loving person,
was noted on the left inner
father and a boyfriend. He is also
ankle and a reddish, grade
the comedian in the family. He is
28. 2 bedsore, one inch in
the eldest among 3 siblings and
diameter, irregular in form
has 4 offsprings; 3 of which are
was noted 1 inch above the
males. He is the provider together
right outer ankle
with his wife but because of his
• with scalings found both
work, he isn’t living together with
on lower extremities
his family but communicates 2-3x/
week through cellular phone. He is
in good terms with his parents,
Date: January 9, 2007 2:30 pm
siblings, girlfriend and friends.
Tuesday
GENOGRAM:
General appearance:
Seen lying on bed, asleep, with
NGT @ left nostril, with FBC
draining well to CDU, with the
following v/s: BP 120/80 mmHg,
PR: 71 bpm, RR: 17 cpm, T:
36.7°C/axilla
SIGIFICANT FINDINGS:
• (-) cardinal and
(-)peripheral gaze
• still can’t see
• with NGT @ left nostril
• presence of tattoo at right
scapular region
• rales in both lung fields
• with FBC draining well to
CDU
• Both upper and lower
29. extremities are still in
9. Sexuality-reproductive
decorticate state
pattern
• A whitish, grade 2
Patient had his
bedsore, half inch in
circumcision at 10 years old at the
diameter, circular in form
health center at Novaliches,
was noted on the left inner
Quezon city. He has no history of
ankle and a reddish, grade
STD. S.O. does not know if the
2 bedsore, one inch in
patient performs TSE and does not
diameter, irregular in form
know the patient's sexual
was noted 1 inch above the
activities.
right outer ankle
10. Coping-stress pattern
• with scalings found both
When asked, S.O
on lower extremities
verbalized that the patient's major
stressors are financial problems
but is able to afford family's needs
Date: January 19, 2007 9:45 am
such as tuition fees, food, etc.
Wednesday
Support comes mainly from family
and close relatives and seeks for
General appearance:
friend's advices. He usually
Seen lying on bed, awake,
relieves stress by resting.
conscious, incoherent, afebrile,
11. Value-belief pattern with NGT @ left nostril, with FBC
Patient is a roman draining well to CDU, with the
catholic. S.O. does not know if the following v/s: BP: 120/80 mmHg,
patient prays everyday and goes to PR: 73 bpm, RR: 18 cpm, T:
mass every Sunday. Patient is not 36.8°C/axilla
involved in any religious
organizations. Patient does not SIGNIFICANT FINDINGS:
have cultural practices that causes
guilt. • (-) cardinal and
(-)peripheral gaze
• still can’t see
Environmental history:
• with NGT @ left nostril
Patient is currrently
30. • presence of tattoo at right
residing at Happy-happy
scapular region
compound, Tisa Labangon, Cebu
• rales in both lung fields
city. According to S.O., this place
• with FBC draining well to
serves as the patient’s office and
CDU
home in Cebu however the S.O.
• Both upper and lower
has not yet been to the patient’s
extremities are still in
place so he can’t further describe
decorticate state
the place.
• with scalings found both
In Pasig, Manila, they
on lower extremities
have been living there for 37
• A whitish, grade 2
years, the house and lot is owned.
bedsore, half inch in
They have been living in a two-
diameter, circular in form
storey house with 4 bedrooms
was noted on the left inner
occupied by 14 people and a
ankle and a reddish, grade
separate room for kitchen and
2 bedsore, one inch in
dining room. It has 6 windows. It
diameter, irregular in form
is beside the main road, 1 meter
was noted 1 inch above the
away from the church, 2 meters
right outer ankle
away from the brgy. Hall, 3 meters
away from the market, and 10
MUSCLE STRENGTH:
meters away from the health
center. Transportation is
1/5 1/5
accessible. They have 1 pet, dog
1/5 1/5 December 13, 18-20,
named Rocky. Water source is
2006
supplied by Nawasa and electricity
is supplied by Meralco.
2/5 2/5
2/5 2/5 January 3, 8-10, 2007
Summary of Significant Summary of Significant Findings:
Findings: PHYSICAL EXAMINATION:
• (-) cardinal and
1. Heredofamilial disease
(-)peripheral gaze
includes hypertension and
31. •
cancer on the paternal side. still can’t see
2. Px is currently on NGT. • with NGT @ left nostril
3. Px has been w/ fbc-cdu • presence of tattoo at right
from Dec. 5-12, 2006 and scapular region
Dec. 14-26, 2006 and • rales in both lung fields
urinates more than 1,000ml • with FBC draining well to
of urine per day with a CDU
dark yellow colored urine.
• Both upper and lower
But was removed last Dec.
extremities are still in
27, 2006 due to the
decorticate state
presence of UTI
• with scalings found both
4. He defecates everyday with
on lower extremities
a yellow watery stool.
• A whitish, grade 2
5. Px is currently always on
bedsore, half inch in
hospital bed and cannot
diameter, circular in form
change positions such as
was noted on the left inner
turning to sides, sitting
ankle and a reddish, grade
down and standing up on
2 bedsore, one inch in
his own.
diameter, irregular in form
was noted 1 inch above the
right outer ankle
LABORATORY:
11/24/06
Urinalysis
Color: straw
RBC: 0-2/hpf
heat & acetic acid: (-)
pH: 6.5
WBC: 0-1/hpf
32. Specific Gravity: 1.006
epithelial cells: 0-2/hpf
Protein: trace
ketone: (-)
Glucose: ++
blood: +
Reducing Substances: ++
amorphous materials: (-)
Purpose:
Means of knowing the various
properties of urine, a routine
procedure for every patient to
determine any pathological
disorders.
Implication:
Presence of protein, glucose,
Reducing substance, blood in urine
and low specific gravity usually
indicates Infection
11/24/06
ECG
Rate: Atrial = 107/min.
Ventricular = 107/ min.
Rhythm: sinus
Axis: (+) 40
PR interval: 0.16 sec.
QRS interval: 0.08 sec.
QT interval: 0.40 sec.
P Wave: low to flat
33. QRS: bizarre complexes seen in
V1, V4 r S R pattern seen in V1,
V2
Transitional zone : V4
T wave: upright
ST segment: isoelectric
Interpretation:
Sinus tachycardia with premature
ventricular contractions,
intraventricular conduction defect.
Non specific ST-T wave changes.
11/27/06
Gram Staining: Gram (+) cocci in
pairs: few/OIF
Pus cells: moderate
11/28/06
Smear Culture: Gram (-) rods
Culture: Acinetobacter iwoffi
Remarks: Sensitivity test result of
culture: A.iwoffi
Purpose:
Allows for morphologic
examination of cells contained in
the specimen and differentiate any
bacteria present, may be used to
differentiate true sputum from
saliva and upper respiratory tract
infections
34. Implication:
Indicates infection of the
respiratory tract secondary to
pneumonia as manifested by
whitish sputum and rales.
12/6/06
Complete Blood Count
Normal Values
WBC ↑17 K/uL
4.10-10.9 K/uL
NEU ↑12.5 73.2%N
2.5-7.5 47-80%N
LYM ↑1.60 ↓9.36%L
1-4 13-40%L
MONO 1.08 6.34% M
1-1.20 2-11%M
EOS. ↑1.78 ↑10.4%E
0-.5 0-5%E
BASO ↑.107 .625% B
0-.1 0-2%B
RBC ↑5.91M/uL
4-5.2M/uL
HGB ↓11.7.0 g/dL
12-16 g/dL
HCT 36.1 %
36-46%
MCV ↓61.1.0 fL
80-100 fL
MCH ↓25.6 pg
26-34 pg
MCHC 32.3 g/dL
35. 31-36 g/dL
RDW 17 %
11.6-18%
PLT 417 K/uL
140-440 K/uL
MPV 7.69 fL
0-100 fL
Purpose:
To determine whether specific
blood levels are higher or lower
than normal and can be useful I the
diagnosis of such diseases such as
anemia, leukemia, and infection
Implication:
An increase in WBC and
neutrophils indicate an infection
secondary to nosocomial
pneumonia and as manifested by
rales and whitish sputum
A decrease in HBG, MCV and
MCHC may indicate red
hepatization secondary nosocomial
pneumonia
An increase in RBC may indicate
dehydration
12/6/06
Creatinine = 1.3 mg/dL
Normal Value (0.5-13 mg/dL)
Purpose:
36. To determine for renal function
Implication:
Within normal range
12 – 6 – 06
Calcium = 4.32 mg %↓
Normal Value (4.6 – 5.16 mg %)
Purpose:
To aid diagnosis of
neuromuscular, skeletal and
endocrine disorder, arrhythmias,
blood clotting deficiencies, acid-
base imbalance.
Implication:
Decrease in calcium levels
indicates hypocalcemia as
manifested by generalized muscle
spasms, as seen in the patient
having decorticate
Potassium = 4.7 mmol/L
Normal Value (4.0 – 5.6 mmol/L)
Sodium = 131 mmol/ L↓
Normal Value (136 – 142 mmol/L)
Purpose:
To evaluate fluid electrolyte and
acid-base balance and related
neuromuscular, renal and adrenal
37. functions
Implication:
Abnormally low serum sodium
levels result from diarrhea
Potassium value is within normal
12/11/06 5:58pm
WBC 11.7 k/ul ↓
NEU 7.25 61.7% N
LYM 2.10 17.9% L
MONO .356 3.03%M
EOS 1.92 16.4%E↑
BASO .114 .970%B
RBC 5.39m/uL
HGB 10.5 g/dL↓
HCT 33.5%↓
MCV 62.2 fL↓
MCH 19.4 pg↓
MCHC 31.3 g/dL
RDW 17.3%
PLT 398 k/uL
MPV 7.47 fL
Implication:
An elevated WBC and Eosinophils
usually signal infection as
manifested by blood in urine,
cloudy appearance
A decreased Hgb, HCT, MCV,
MCH indicates red hepatization
secondary to nosocomial
38. pneumonia
12/26/06
Urinalysis
Color: yellow
Appearance: cloudy
RBC: 5-10/hpf
heat & acetic acid: (+)
pH: 6.5
WBC: 30-40/hpf
Bacteria: moderate
Specific Gravity: 1.020
epithelial cells: 2-5/hpf
Protein: 30(++ )
ketone: (-)
Glucose(-)
blood: moderate(++)
Reducing Substances:(-)
amorphous materials: urates: rare
Purpose:
Means of knowing the various
properties of urine, a routine
procedure for every patient to
determine any pathological
disorders.
Implication:
Cloudy urine, proteinuria,
Increased WBC, presence of
epitheilai cells and bacteria
indicates infection secondary
40. 11/24/06
Urinalysis
RBC: 0-2/hpf
pH: 6.5
WBC: 0-1/hpf
epithelial cells: 0-2/hpf
Protein: trace
Glucose:++
blood: +
Reducing Substances:++
amorphous materials: (-)
12/26/06
Urinalysis
RBC: 5-10/hpf
heat & acetic acid: (+)
WBC: 30-40/hpf
Bacteria: moderate
epithelial cells: 2-5/hpf
Protein: 30(++ )
blood: moderate(++)
amorphous materials: urates: rare
11/24/06
ECG
QRS : bizarre complexes seen
in V1, V4 r S R pattern seen in V1,
V2
12 – 6 – 06
41. Results
Normal Values
Calcium = 4.32 mg %↓
4.6 – 5.16 mg %
Sodium = 131 mmol/ L↓
136 – 142 mmol/L
12/11/06 5:58pm
WBC 11.7 k/ul ↓
EOS 1.92 16.4%E↑
HGB 10.5 g/dL↓
HCT 33.5%↓
MCV 62.2 fL↓
MCH 19.4 pg↓
11/27/06
Gram Staining: Gram (+) cocci in
pairs: few/OIF
Pus cells: moderate
11/28/06
Smear Culture: Gram (-) rods
Culture: Acinetobacter iwoffi
Remarks: Sensitivity test result of
culture: A.iwoffi
KEY ISSUES
December 13, 2006 Desired Outcome:
Independent Interventions: Within 8 hours of nursing
1. Ineffective airway clearance 1. Auscultated chest, noted presence of intervention, the patient:
• will be able to maintain
related to excessive secretions and adventitious breath sounds and presence of
prolonged immobility 2˚ to secretions patent airway and will be
42. nosocomial pneumonia as R: Provides information regarding inflow through clear from secretions
•
manifested by presence of the airway and the presence or absence of fluid able to breathe
productive cough with whitish mucus obstruction independently without
sputum, with rales heard on both 2. Monitored respiratory rate and noted presence Oxygen therapy,
lung fields upon auscultation, use of dyspnea, Tachypnea, or reports of air hunger • will manifest clear lung
of accessory muscles (subcostal), and use of accessory muscles. sounds
restlessness, O2 at 2L/min, noisy R: Tachypnea might further develop to • no longer use of accessory
breathing and a culture of gram (-) respiratory distress. muscles in breathing,
rods of Acinetobacter iwoffi 3. Observed sputum noting color, odor and • will have a respiratory rate
volume within the range of 14-
Scientific Basis: R: Normal sputum is clear or gray and minimal; 20cpm
Immobilized clients and those on abnormal sputum is green, yellow or bloody, • will no longer manifest
bed rest are generally weakened. If malodorous and often copious restlessness and noisy
weakness progresses, the cough 4. Maintained a moderate high back rest position, breathing
reflex gradually becomes positioned head midline with flexion
inefficient. The stasis of secretions R: Lessen pressure on lungs allowing more room Actual Outcome:
in the lungs may be life for expansion 12/13/06
threatening for an immobilized 5. Elevated head of bed with the use of pillows. After 8 hours of nursing
client since pneumonia can easily R: Stimulates respiratory functioning or lung intervention, the client manifested
develop. (Fundamentals of expansion the ff:
Nursing, Potter and Perry 6th Ed 6. Provided oral care every four hours
• whitish sputum was present
pg. 1451) R: Oral care freshens the mouth after respiratory
• Strong rales were heard at both
secretions have been expectorated
lung fields
• used accessory muscles for
Collaborative Interventions:
breathing
1. Suctioned PRN
• O2 was on at 2LPM
R: Suctioning clears the airway from secretions,
• RR was at 16 cpm
thus promoting better airway passage.
2. Administered O2 inhalation via nasal cannula
12/18/06
at 2L/min.
After 8 hours of nursing
R: Maintain adequate O2 supply, and prevent
intervention, the client manifested
hypoxia.
the ff:
3. Administered Salbuterol(Salbutamol) 1/2 neb +
43. • Sputum was present
2cc NSS q 8hrs
R: Bronchodilators; relaxes bronchial, uterine and • Strong rales were still heard at
vascular smooth muscles by stimulating the beta2 both lung fields
receptors • Still used accessory muscles
5. Performed Chest Physiotherapy after for breathing
nebulization for 15 minutes • O2 was on at 2LPM
R: To encourage loosening and expectoration of • RR was 20 cpm
mucus from the respiratory tract through the
postural gravity drainage and percussion and 12/19-20/06, 01/03/07
vibrating techniques After 8 hours of nursing
intervention, the client manifested
the ff:
• Minimal rales were heard at
both lung fields
• Still used accessory muscles
for breathing
• RR was within normal range
• Sputum was present
12/28/06
After 8 hours of nursing
intervention, the client manifested
the ff:
• O2 was out of bedside
01/08-10/07
After 8 hours of nursing
intervention, the client manifested
the ff:
• Strong rales were heard at both
lung fields
44. • Still used accessory muscles
for breathing
• O2 was out of bedside
• Sputum was present
• RR was within normal range
2. Ineffective breathing pattern Independent Interventions: Desired Outcome:
related to neuromuscular 1. Monitored respiratory rate, depth and effort. Within 8 hours of nursing
dysfunction and retained R: Dyspnea may be present because of hypoxia interventions,
secretions 2˚ nosocomial 2. Auscultated breath sounds, noting crackles on the patient:
• will show improved
pneumonia as manifested by use both lung fields.
of accessory muscles (subcostal), R: Indicates developing complications, increasing respiratory pattern
shortness of breath, noisy risk of infection. • will lessen use of
breathing pattern and O2 at 2LPM 3. Maintained MHBR position by placing 2 accessory muscles
pillows under head when lying down. • have RR within normal
SB: The onset of all pneumonias is R: Facilitates breathing by reducing pressure on range 14-20cpm
generally marked by any or all of the diaphragm and minimizes risk of aspiration of • Will no longer manifest
the following manifestations: secretions shortness of breath and
fever, chills, sweats, pleuritic chest 4. Encouraged adequate rest and limit activities noisy breathing pattern
pain, cough, sputum production, within client tolerance.
hemoptysis, increased in R: Helps limit oxygen needs/consumption. Actual Outcome:
respiration, dyspnea, headache, 12/13/06, 12/18-20/06
and fatigue. (Medical-Surgical Collaborative Interventions: After 8 hours of nursing
Nursing 6th Edition page 1713 by 1. Suctioned PRN intervention, the client manifested
Joyce M. Black) R: Suctioning clears the airway from secretions, the ff:
thus promoting better airway passage. • Still used accessory muscles
2. Administered O2 inhalation via nasal cannula for breathing
at 2L/min.
• O2 was on at 2LPM
R: Maintain adequate O2 supply, and prevent
• RR was within normal range
hypoxia.
• Noisy breathing and shortness
3. Administered Salbuterol(Salbutamol) 1/2 neb +
of breath
2cc NSS q 8hrs
R: Bronchodilators; relaxes bronchial, uterine and
45. vascular smooth muscles by stimulating the beta2 01/03/07, 01/08-10/07
receptors After 8 hours of nursing
4. Performed Chest Physiotherapy after intervention, the client manifested
nebulization for 15 minutes the ff:
• Still used accessory muscles
R: To encourage loosening and expectoration of
mucus from the respiratory tract through the for breathing
postural gravity drainage and percussion and • O2 was out of bedside
vibrating techniques • RR was within normal range
• Noisy breathing and shortness
of breath was no longer
present
3. Risk for Aspiration Independent Interventions: Desired Outcome:
Cues: 1. Noted client’s level of consciousness Within 8 hours of nursing
• Presence of NGT R: To assess causative/contributing factors intervention, the patient:
• will be able to experience
2. Assessed RR
• Impaired swallowing
R: To assist in correcting factors that can lead to no aspiration as evidenced
• Reduced level of
aspiration by noiseless respiration,
consciousness with the GCS
3. Check gag reflex clear breath sounds
of 6 (E-4, M-1, V-1)
R: To assist in correcting factors that can lead to • maintain patent airway
aspiration The SO:
Scientific Basis:
4. Assessed the Glasgow coma scale of the • will follow correct
A serious complication associated
patient.
with enteral feeding is aspiration instructions regarding NGT
R: To assist in correcting factors that can lead to
of formula into the feeding
aspiration
tracheobronchial tree. Aspiration
5. Auscultated for gurgling sounds in the stomach
of enteral formula into the lungs Actual Outcome:
prior to NGT feeding
irritates the bronchial mucosa, 12/13, 12/18-20, 01/03, 01/08-10
R: To ensure patency of NGT
resulting in decreased blood After 8 hours of nursing
6. Suction client before NGT feeding
supply to affected pulmonary intervention, the client manifested
R: To prevent aspiration of ingested food
tissues. (Fundamentals of Nursing, the ff:
7. Positioned client in a high Fowler’s position • Was positioned at high
Potter and Perry 6th Ed pg. 1304)
before feeding Fowler’s prior to every NGT
R: To prevent aspiration if ingested food feeding and patency of the