This document provides information on various metabolic emergencies that oncologists may encounter, including tumour lysis syndrome, hyponatremia, hypercalcemia, lactic acidosis, and hyperammonia. It focuses on sodium disorders and discusses hyponatremia and hypernatremia in depth. Hyponatremia is a common condition in cancer patients that can be caused by the disease, medications, or comorbidities. It outlines approaches for screening, diagnosis, classification, and management of hyponatremia depending on the severity and chronicity of the low sodium levels. Rapid correction of sodium is important in acute severe cases to avoid neurological complications.
This document discusses the approach to hypo- and hypernatremia in neurosurgical patients in the perioperative period. It covers several key points:
1. Hyponatremia is common in neurosurgical patients and is associated with high mortality. It can be categorized based on extracellular fluid volume status. SIADH and cerebral salt wasting require different treatments.
2. Hypernatremia results from a loss of free water and can cause central nervous system dysfunction. Rapid correction poses risks like cerebral edema. The approach involves assessing volume status based on labs and symptoms.
3. Diabetes insipidus is a potential complication after pituitary or brain surgeries/injuries. It involves excessive
This document discusses hyponatremia and hypernatremia. It begins by explaining sodium regulation and the physiological basis of serum sodium concentration. It then defines and describes the types and causes of hyponatremia, including hypovolemic, euvolemic, and hypervolemic hyponatremia as well as pseudo hyponatremia. Specific conditions like SIADH are explained in detail. The clinical features, diagnosis, and treatment of hyponatremia are outlined. Hypernatremia is also defined and its causes such as net water loss or hypertonic sodium gain are summarized. The clinical features of hypernatremia are said to be predominantly neurologic.
This document discusses hyponatremia and hypernatremia. It begins by explaining sodium regulation and the physiological basis of serum sodium concentration. It then defines and describes the types and causes of hyponatremia, including hypovolemic, euvolemic, and hypervolemic hyponatremia as well as pseudo hyponatremia. Specific conditions like SIADH are explained in detail. The clinical features, diagnosis, and treatment of hyponatremia are outlined. Hypernatremia is also defined and the causes of net water loss and hypertonic sodium gain are listed. The clinical features of hypernatremia are said to be predominantly neurologic.
Sodium homeostasis and the regulation of serum sodium concentration is essential for normal physiological functioning. Hyponatremia occurs when there is a relative excess of water compared to sodium, decreasing the plasma sodium concentration below 135 mmol/L. It can be hypo-osmolar, euvolemic, or hypervolemic depending on water and sodium levels. Treatment involves correcting the underlying cause, restricting water intake, and sometimes using hypertonic saline or vaptans. Rapid correction of sodium levels can have neurological consequences, so changes should be gradual. Hypernatremia is less common but also dangerous, defined as a sodium level over 145 mmol/L.
Hyponatremia is defined as a low serum sodium concentration and can be acute (<48 hours) or chronic (>48 hours). It is clinically important because acute severe hyponatremia can cause morbidity and mortality, and adverse outcomes are higher in hyponatremic patients. Overly rapid correction of chronic hyponatremia can cause severe neurological deficits or death. Hyponatremia can be hypervolemic, hypovolemic, or euvolemic based on water and sodium levels. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common cause of euvolemic hyponatremia and results from excess vasopressin secretion. Treatment depends on
This document discusses sodium imbalance and hyponatremia. It provides details on:
- Normal sodium regulation and the causes of hyponatremia being related to water excess relative to sodium.
- The approach to evaluating hyponatremia by measuring osmolality, estimating volume status, and getting urinary sodium and osmolality levels.
- Specific causes of hyponatremia like SIADH, cerebral salt wasting, and mineralocorticoid deficiency.
- The treatment of hyponatremia depending on if it is acute or chronic and correcting it slowly to avoid osmotic demyelination syndrome.
Hyponatremia is a common electrolyte abnormality seen in clinical practice. It is defined as a serum sodium level below 135 mmol/L. The main types are isotonic, hypertonic, and hypotonic hyponatremia. Causes include diuretic use, liver cirrhosis, heart failure, and SIADH. Diagnosis involves lab tests and imaging. Management depends on severity and rate of onset, with slow correction for chronic cases to avoid osmotic demyelination syndrome. Fluid restriction and vasopressin antagonists are often used to treat euvolemic hyponatremia.
Hypokalemia, or low potassium levels, can be caused by inadequate intake, excessive losses, or impaired renal excretion. Common symptoms include muscle weakness, constipation, and cardiac arrhythmias. Evaluation involves checking renal function tests and electrolyte levels. Management focuses on replacing potassium losses through oral or intravenous supplementation depending on the severity. Close monitoring is needed to prevent overcorrection.
This document discusses the approach to hypo- and hypernatremia in neurosurgical patients in the perioperative period. It covers several key points:
1. Hyponatremia is common in neurosurgical patients and is associated with high mortality. It can be categorized based on extracellular fluid volume status. SIADH and cerebral salt wasting require different treatments.
2. Hypernatremia results from a loss of free water and can cause central nervous system dysfunction. Rapid correction poses risks like cerebral edema. The approach involves assessing volume status based on labs and symptoms.
3. Diabetes insipidus is a potential complication after pituitary or brain surgeries/injuries. It involves excessive
This document discusses hyponatremia and hypernatremia. It begins by explaining sodium regulation and the physiological basis of serum sodium concentration. It then defines and describes the types and causes of hyponatremia, including hypovolemic, euvolemic, and hypervolemic hyponatremia as well as pseudo hyponatremia. Specific conditions like SIADH are explained in detail. The clinical features, diagnosis, and treatment of hyponatremia are outlined. Hypernatremia is also defined and its causes such as net water loss or hypertonic sodium gain are summarized. The clinical features of hypernatremia are said to be predominantly neurologic.
This document discusses hyponatremia and hypernatremia. It begins by explaining sodium regulation and the physiological basis of serum sodium concentration. It then defines and describes the types and causes of hyponatremia, including hypovolemic, euvolemic, and hypervolemic hyponatremia as well as pseudo hyponatremia. Specific conditions like SIADH are explained in detail. The clinical features, diagnosis, and treatment of hyponatremia are outlined. Hypernatremia is also defined and the causes of net water loss and hypertonic sodium gain are listed. The clinical features of hypernatremia are said to be predominantly neurologic.
Sodium homeostasis and the regulation of serum sodium concentration is essential for normal physiological functioning. Hyponatremia occurs when there is a relative excess of water compared to sodium, decreasing the plasma sodium concentration below 135 mmol/L. It can be hypo-osmolar, euvolemic, or hypervolemic depending on water and sodium levels. Treatment involves correcting the underlying cause, restricting water intake, and sometimes using hypertonic saline or vaptans. Rapid correction of sodium levels can have neurological consequences, so changes should be gradual. Hypernatremia is less common but also dangerous, defined as a sodium level over 145 mmol/L.
Hyponatremia is defined as a low serum sodium concentration and can be acute (<48 hours) or chronic (>48 hours). It is clinically important because acute severe hyponatremia can cause morbidity and mortality, and adverse outcomes are higher in hyponatremic patients. Overly rapid correction of chronic hyponatremia can cause severe neurological deficits or death. Hyponatremia can be hypervolemic, hypovolemic, or euvolemic based on water and sodium levels. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common cause of euvolemic hyponatremia and results from excess vasopressin secretion. Treatment depends on
This document discusses sodium imbalance and hyponatremia. It provides details on:
- Normal sodium regulation and the causes of hyponatremia being related to water excess relative to sodium.
- The approach to evaluating hyponatremia by measuring osmolality, estimating volume status, and getting urinary sodium and osmolality levels.
- Specific causes of hyponatremia like SIADH, cerebral salt wasting, and mineralocorticoid deficiency.
- The treatment of hyponatremia depending on if it is acute or chronic and correcting it slowly to avoid osmotic demyelination syndrome.
Hyponatremia is a common electrolyte abnormality seen in clinical practice. It is defined as a serum sodium level below 135 mmol/L. The main types are isotonic, hypertonic, and hypotonic hyponatremia. Causes include diuretic use, liver cirrhosis, heart failure, and SIADH. Diagnosis involves lab tests and imaging. Management depends on severity and rate of onset, with slow correction for chronic cases to avoid osmotic demyelination syndrome. Fluid restriction and vasopressin antagonists are often used to treat euvolemic hyponatremia.
Hypokalemia, or low potassium levels, can be caused by inadequate intake, excessive losses, or impaired renal excretion. Common symptoms include muscle weakness, constipation, and cardiac arrhythmias. Evaluation involves checking renal function tests and electrolyte levels. Management focuses on replacing potassium losses through oral or intravenous supplementation depending on the severity. Close monitoring is needed to prevent overcorrection.
This document discusses a case of a 68-year-old female smoker presenting with malaise and poor appetite. Lab results showed hyponatremia. A CT scan revealed a right lung nodule. The patient was diagnosed with SIADH secondary to the lung mass. The document then provides details on hyponatremia, the approach to evaluating and treating a patient with hyponatremia including the role of arginine vasopressin, SIADH, and treatment strategies such as fluid restriction, demeclocycline, urea, lithium, and the non-peptide vasopressin receptor antagonist tolvaptan. It summarizes results from the SALT trials demonstrating tolv
This document discusses a case of a 68-year-old female smoker presenting with malaise and poor appetite. Lab results showed hyponatremia. A CT scan revealed a right lung nodule. The patient was diagnosed with SIADH secondary to the lung mass. The document then provides details on hyponatremia, the approach to evaluating and treating a patient with hyponatremia including the role of arginine vasopressin, SIADH, and treatment strategies such as fluid restriction, demeclocycline, urea, lithium, and the non-peptide vasopressin receptor antagonist tolvaptan. It summarizes results from the SALT trials demonstrating tolv
This document discusses hyponatremia, defined as a plasma sodium concentration less than 135 mEq/L. It describes the etiology and pathogenesis of hyponatremia as being related to the kidney's inability to excrete water or excess water intake. The classification of hyponatremia includes pseudohyponatremia, hyperosmolar hyponatremia, and true hyponatremia. The treatment of hyponatremia depends on whether it is acute or chronic, symptomatic or asymptomatic, and the underlying cause. The rate of sodium correction is an important consideration to avoid complications like central pontine myelinolysis.
This document discusses electrolytes, specifically sodium disorders like hyponatremia and hypernatremia. It defines hyponatremia as a plasma sodium concentration below 135 mM and divides it into three categories based on volume status: hypovolemic, euvolemic, and hypervolemic. Common causes of euvolemic hyponatremia include syndrome of inappropriate antidiuretic hormone secretion. Treatment depends on symptoms and involves slow correction to avoid osmotic demyelination syndrome. Vaptan antagonists and fluid restriction are effective therapies. Hypernatremia occurs when sodium levels rise above 145 mM due to water loss exceeding sodium loss.
The document discusses hyponatremia, defining it as a low serum sodium concentration and describing the physiology and pathophysiology of sodium regulation in the body. It examines the epidemiology, classification, clinical manifestations, diagnosis, and treatment of hyponatremia, providing details on evaluating volume status, calculating sodium deficits, and correcting sodium levels based on chronicity and symptoms.
1. Hyponatremia is defined as a serum sodium level below 135 mEq/L and can be classified as mild, moderate, or severe based on the serum sodium concentration.
2. Signs and symptoms range from nausea and malaise in mild cases to seizures and coma in severe cases and depend on the severity and chronicity of hyponatremia.
3. Causes of hyponatremia include excessive water intake, syndrome of inappropriate antidiuretic hormone secretion, and conditions affecting sodium balance such as liver disease, heart failure, and use of certain medications.
This document summarizes common electrolyte disturbances including sodium, potassium, calcium and magnesium abnormalities. It discusses causes, signs/symptoms, evaluation and treatment of hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia and hypomagnesemia. Evaluation involves assessing volume status, determining the cause, and measuring electrolyte and osmolarity levels. Treatment aims to address the underlying cause and correct electrolyte abnormalities slowly to avoid complications.
This document discusses guidelines for the diagnosis and management of hyponatremia according to NICE. It defines hyponatremia as a sodium level below 135 mEq/L and describes its causes including hypovolemic, hypervolemic, and euvolemic types. It outlines approaches to evaluating volume status and correcting sodium levels, noting the importance of avoiding rapid overcorrection to prevent osmotic demyelination syndrome. Treatment involves fluid restriction, hypertonic saline in severe cases, and addressing underlying causes such as SIADH. Special considerations are given for cirrhosis, adrenal insufficiency, and drug-induced hyponatremia.
The document discusses electrolyte imbalances and their neurology. It covers sodium, potassium, calcium and magnesium disorders. For sodium, it describes hyponatremia and hypernatremia in detail. Hyponatremia can be hypovolaemic, hypervolaemic or euvoleamic. Causes, clinical features and treatment approaches are provided. For potassium, it discusses hypokalemia and its neuromuscular and cardiac manifestations. Causes of hypokalemia include reduced intake, renal and non-renal losses, and intracellular shifting. ECG changes are also outlined.
This document discusses various electrolyte abnormalities including sodium, potassium, calcium and magnesium disorders. It provides definitions, epidemiology, causes, clinical features and treatment approaches for conditions like hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypercalcemia and hypocalcemia. Specifically, it outlines the evaluation and management of sodium disorders like hyponatremia and hypernatremia due to various volume status abnormalities.
Hyponatremia is defined as a serum sodium concentration below 135 mEq/L. It is commonly seen in hospitalized patients and those with conditions like heart failure, cirrhosis, and SIADH. Treatment involves correcting the underlying cause and raising the serum sodium level, but too rapid of a correction can cause serious neurological complications. Tolvaptan is a vasopressin receptor antagonist that promotes water excretion without electrolyte loss, allowing for a safe correction of hyponatremia within 24-48 hours. Clinical trials demonstrated its ability to significantly increase serum sodium levels compared to placebo.
This document discusses hyponatremia (low sodium levels in blood). It begins by defining relevant terms like osmolality and normal ranges. It then notes that hyponatremia is most common in females, elderly, and hospitalized patients. The diagnosis involves assessing volume status, serum osmolality, and urine sodium and osmolality. Treatment depends on the cause but aims to slowly correct sodium levels to prevent central pontine myelinolysis, a severe neurological condition.
This document summarizes electrolyte disturbances, specifically disorders of sodium and potassium balance. It discusses the causes, types, clinical features, diagnosis, and treatment of hyponatremia, hypernatremia, hypokalemia, and hyperkalemia. The key points covered include normal sodium and potassium levels, how they are regulated, complications that can arise from imbalances, and goals and principles of correcting electrolyte abnormalities.
1. Hyponatremia is defined as a serum sodium below 135 mmol/L and is the most common electrolyte disorder seen in clinical practice.
2. The document discusses the etiologies and pathophysiologies of hyponatremia including hypovolemic, euvolemic, and hypervolemic causes.
3. Treatment of hyponatremia depends on the severity and chronicity of the low sodium levels and involves restricting water intake, sodium supplementation, or in severe cases, hypertonic saline therapy. The goal is to correct sodium levels slowly to avoid osmotic demyelination syndrome.
- Hyponatremia in ICU patients is commonly caused by inappropriate secretion of antidiuretic hormone leading to retention of free water.
- The brain adapts slowly to changes in serum sodium levels over 48 hours; rapid corrections can cause serious complications like osmotic demyelination syndrome.
- Treatment goals for hyponatremia are to correct the sodium level slowly at a rate of no more than 6 mEq/L per day to prevent neurological complications while relieving symptoms.
This document discusses hyponatremia, defined as a plasma sodium concentration less than 135mM. Hyponatremia is common, occurring in up to 22% of hospitalized patients and 15% of general admissions. It can be associated with poor outcomes if left untreated. The mechanism is usually an increase in arginine vasopressin leading to water retention. Causes include SIADH, heart failure, liver cirrhosis, and use of certain drugs. Treatment involves restricting water intake, replacing sodium deficits, and treating the underlying cause. Rapid correction of sodium levels should be avoided to prevent neurological complications.
Hyponatremia is defined as a serum sodium concentration below 135 meq/L. The serum sodium concentration is determined by the balance of sodium and other electrolytes in the total body water. Hyponatremia can be classified as hypovolaemic, euvolemic, or hypervolaemic based on volume status. Common causes include syndrome of inappropriate antidiuretic hormone secretion, heart failure, liver cirrhosis, and use of thiazide diuretics. Symptoms range from nausea and headache with acute hyponatremia to more severe symptoms like seizures and coma. Treatment involves correcting underlying causes and raising serum sodium levels slowly to avoid osmotic demyelination
This document discusses a case of a 68-year-old female smoker presenting with malaise and poor appetite. Lab results showed hyponatremia. A CT scan revealed a right lung nodule. The patient was diagnosed with SIADH secondary to the lung mass. The document then provides details on hyponatremia, the approach to evaluating and treating a patient with hyponatremia including the role of arginine vasopressin, SIADH, and treatment strategies such as fluid restriction, demeclocycline, urea, lithium, and the non-peptide vasopressin receptor antagonist tolvaptan. It summarizes results from the SALT trials demonstrating tolv
This document discusses a case of a 68-year-old female smoker presenting with malaise and poor appetite. Lab results showed hyponatremia. A CT scan revealed a right lung nodule. The patient was diagnosed with SIADH secondary to the lung mass. The document then provides details on hyponatremia, the approach to evaluating and treating a patient with hyponatremia including the role of arginine vasopressin, SIADH, and treatment strategies such as fluid restriction, demeclocycline, urea, lithium, and the non-peptide vasopressin receptor antagonist tolvaptan. It summarizes results from the SALT trials demonstrating tolv
This document discusses hyponatremia, defined as a plasma sodium concentration less than 135 mEq/L. It describes the etiology and pathogenesis of hyponatremia as being related to the kidney's inability to excrete water or excess water intake. The classification of hyponatremia includes pseudohyponatremia, hyperosmolar hyponatremia, and true hyponatremia. The treatment of hyponatremia depends on whether it is acute or chronic, symptomatic or asymptomatic, and the underlying cause. The rate of sodium correction is an important consideration to avoid complications like central pontine myelinolysis.
This document discusses electrolytes, specifically sodium disorders like hyponatremia and hypernatremia. It defines hyponatremia as a plasma sodium concentration below 135 mM and divides it into three categories based on volume status: hypovolemic, euvolemic, and hypervolemic. Common causes of euvolemic hyponatremia include syndrome of inappropriate antidiuretic hormone secretion. Treatment depends on symptoms and involves slow correction to avoid osmotic demyelination syndrome. Vaptan antagonists and fluid restriction are effective therapies. Hypernatremia occurs when sodium levels rise above 145 mM due to water loss exceeding sodium loss.
The document discusses hyponatremia, defining it as a low serum sodium concentration and describing the physiology and pathophysiology of sodium regulation in the body. It examines the epidemiology, classification, clinical manifestations, diagnosis, and treatment of hyponatremia, providing details on evaluating volume status, calculating sodium deficits, and correcting sodium levels based on chronicity and symptoms.
1. Hyponatremia is defined as a serum sodium level below 135 mEq/L and can be classified as mild, moderate, or severe based on the serum sodium concentration.
2. Signs and symptoms range from nausea and malaise in mild cases to seizures and coma in severe cases and depend on the severity and chronicity of hyponatremia.
3. Causes of hyponatremia include excessive water intake, syndrome of inappropriate antidiuretic hormone secretion, and conditions affecting sodium balance such as liver disease, heart failure, and use of certain medications.
This document summarizes common electrolyte disturbances including sodium, potassium, calcium and magnesium abnormalities. It discusses causes, signs/symptoms, evaluation and treatment of hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia and hypomagnesemia. Evaluation involves assessing volume status, determining the cause, and measuring electrolyte and osmolarity levels. Treatment aims to address the underlying cause and correct electrolyte abnormalities slowly to avoid complications.
This document discusses guidelines for the diagnosis and management of hyponatremia according to NICE. It defines hyponatremia as a sodium level below 135 mEq/L and describes its causes including hypovolemic, hypervolemic, and euvolemic types. It outlines approaches to evaluating volume status and correcting sodium levels, noting the importance of avoiding rapid overcorrection to prevent osmotic demyelination syndrome. Treatment involves fluid restriction, hypertonic saline in severe cases, and addressing underlying causes such as SIADH. Special considerations are given for cirrhosis, adrenal insufficiency, and drug-induced hyponatremia.
The document discusses electrolyte imbalances and their neurology. It covers sodium, potassium, calcium and magnesium disorders. For sodium, it describes hyponatremia and hypernatremia in detail. Hyponatremia can be hypovolaemic, hypervolaemic or euvoleamic. Causes, clinical features and treatment approaches are provided. For potassium, it discusses hypokalemia and its neuromuscular and cardiac manifestations. Causes of hypokalemia include reduced intake, renal and non-renal losses, and intracellular shifting. ECG changes are also outlined.
This document discusses various electrolyte abnormalities including sodium, potassium, calcium and magnesium disorders. It provides definitions, epidemiology, causes, clinical features and treatment approaches for conditions like hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypercalcemia and hypocalcemia. Specifically, it outlines the evaluation and management of sodium disorders like hyponatremia and hypernatremia due to various volume status abnormalities.
Hyponatremia is defined as a serum sodium concentration below 135 mEq/L. It is commonly seen in hospitalized patients and those with conditions like heart failure, cirrhosis, and SIADH. Treatment involves correcting the underlying cause and raising the serum sodium level, but too rapid of a correction can cause serious neurological complications. Tolvaptan is a vasopressin receptor antagonist that promotes water excretion without electrolyte loss, allowing for a safe correction of hyponatremia within 24-48 hours. Clinical trials demonstrated its ability to significantly increase serum sodium levels compared to placebo.
This document discusses hyponatremia (low sodium levels in blood). It begins by defining relevant terms like osmolality and normal ranges. It then notes that hyponatremia is most common in females, elderly, and hospitalized patients. The diagnosis involves assessing volume status, serum osmolality, and urine sodium and osmolality. Treatment depends on the cause but aims to slowly correct sodium levels to prevent central pontine myelinolysis, a severe neurological condition.
This document summarizes electrolyte disturbances, specifically disorders of sodium and potassium balance. It discusses the causes, types, clinical features, diagnosis, and treatment of hyponatremia, hypernatremia, hypokalemia, and hyperkalemia. The key points covered include normal sodium and potassium levels, how they are regulated, complications that can arise from imbalances, and goals and principles of correcting electrolyte abnormalities.
1. Hyponatremia is defined as a serum sodium below 135 mmol/L and is the most common electrolyte disorder seen in clinical practice.
2. The document discusses the etiologies and pathophysiologies of hyponatremia including hypovolemic, euvolemic, and hypervolemic causes.
3. Treatment of hyponatremia depends on the severity and chronicity of the low sodium levels and involves restricting water intake, sodium supplementation, or in severe cases, hypertonic saline therapy. The goal is to correct sodium levels slowly to avoid osmotic demyelination syndrome.
- Hyponatremia in ICU patients is commonly caused by inappropriate secretion of antidiuretic hormone leading to retention of free water.
- The brain adapts slowly to changes in serum sodium levels over 48 hours; rapid corrections can cause serious complications like osmotic demyelination syndrome.
- Treatment goals for hyponatremia are to correct the sodium level slowly at a rate of no more than 6 mEq/L per day to prevent neurological complications while relieving symptoms.
This document discusses hyponatremia, defined as a plasma sodium concentration less than 135mM. Hyponatremia is common, occurring in up to 22% of hospitalized patients and 15% of general admissions. It can be associated with poor outcomes if left untreated. The mechanism is usually an increase in arginine vasopressin leading to water retention. Causes include SIADH, heart failure, liver cirrhosis, and use of certain drugs. Treatment involves restricting water intake, replacing sodium deficits, and treating the underlying cause. Rapid correction of sodium levels should be avoided to prevent neurological complications.
Hyponatremia is defined as a serum sodium concentration below 135 meq/L. The serum sodium concentration is determined by the balance of sodium and other electrolytes in the total body water. Hyponatremia can be classified as hypovolaemic, euvolemic, or hypervolaemic based on volume status. Common causes include syndrome of inappropriate antidiuretic hormone secretion, heart failure, liver cirrhosis, and use of thiazide diuretics. Symptoms range from nausea and headache with acute hyponatremia to more severe symptoms like seizures and coma. Treatment involves correcting underlying causes and raising serum sodium levels slowly to avoid osmotic demyelination
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
NAVIGATING THE HORIZONS OF TIME LAPSE EMBRYO MONITORING.pdfRahul Sen
Time-lapse embryo monitoring is an advanced imaging technique used in IVF to continuously observe embryo development. It captures high-resolution images at regular intervals, allowing embryologists to select the most viable embryos for transfer based on detailed growth patterns. This technology enhances embryo selection, potentially increasing pregnancy success rates.
DECLARATION OF HELSINKI - History and principlesanaghabharat01
This SlideShare presentation provides a comprehensive overview of the Declaration of Helsinki, a foundational document outlining ethical guidelines for conducting medical research involving human subjects.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
10 Benefits an EPCR Software should Bring to EMS Organizations Traumasoft LLC
The benefits of an ePCR solution should extend to the whole EMS organization, not just certain groups of people or certain departments. It should provide more than just a form for entering and a database for storing information. It should also include a workflow of how information is communicated, used and stored across the entire organization.
Summer is a time for fun in the sun, but the heat and humidity can also wreak havoc on your skin. From itchy rashes to unwanted pigmentation, several skin conditions become more prevalent during these warmer months.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
chemistry investigatory project
The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
2. • Metabolic emergencies continue to be an important
challenge for practicing oncologists. Whereas many of
these are well-known side effects of treatments and
individual cancers, others have emerged because of new
and innovative therapies.
• It is essential to anticipate and recognize early signs and
institute appropriate treatment to avoid severe
complications.
7. REGULATION OF BODY WATER
Increased
ECF water
Restoration of
ECF osmolality
Increased water
intake
Stimulation of
hypothalamic
centre
Renal
water
retention
Redistributi
on of water
from ICF
Stimulation of
vasopressin
release
Increased plasma
osmolality
Water loss
8. Overview of Na+ Reabsorption along the
Nephron
65% of filtered Na+ is reabsorbed
from the proximal tubule.
25% of filtered Na+ is reabsorbed
from the thick ascending limb.
5% of filtered Na+ is reabsorbed
from the distal tubule.
4-5% of filtered Na+ is reabsorbed
from the collecting duct.
9. Hyponatremia
Incidence and Etiology
Hyponatremia (serum sodium <135 mmol/L) is a common condition
affecting up to 47% of hospitalized cancer patients.
The incidence of moderate or severe hyponatremia (<130 mmol/L) is
less common (7.8%) but represents levels that are more likely to
be symptomatic (nausea, vomiting, pain, depression, fatigue, and
coma).
The causes of hyponatremia include the disease itself, concomitant
comorbidities, physical stress, and medication.
10. Clinical Features of Hyponatremia
• Acute and Severe –Symptomatic
• Chronic and Mild -Asymptomatic
Hyponatremia
Mild Moderate Severe
Anorexia
Headache
Nausea
Vomiting
Lethargy
Personality change
Muscle Cramps
Muscular
weakness
Confusion
Ataxia
Drowsiness
Diminished Reflexes
Convulsion
Coma & Death
11. It may be a prognostic factor, not only in the case of small-cell lung
cancer but also in other malignancies and is often the result of a
syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
This can occur due to ectopic secretion from the cancer itself or
antidiuretic hormone secretion induced by various medications
including vincristine, cyclophosphamide, opioids, and antidepressants.
12. Other causes hyponatremia include diarrhea and vomiting-induced
hypovolemic hyponatremia, which require volume repletion as a
primary treatment.
Plasma osmolality is closely related to sodium levels and is normally
tightly regulated in the range of 280 to 295mOsm/kg through thirst
perception, control of free water clearance in the kidney by ADH, and
renal sodium excretion regulated by atrial natriuretic peptide and the
renin–angiotensin system.
Therefore,inappropriate or ectopic secretion of either ADH or atrial
natriuretic peptide can result in hyponatremia.
14. Screening, Diagnosis, and
Management
The finding of hyponatremia on a serum chemistry panel does
not necessarily constitute an emergency. However, an appropriate
workup should ensue to determine the cause.
Rapid onset of hyponatremia with refractory seizures and coma can
have a significant mortality, and profound hyponatremia is a true
oncology emergency.
Traditionally, hyponatremia can be classified as hypovolemic,
euvolemic, or hypervolemic; however, this is often difficult to assess
in clinical practice. Often, more than one mechanism is involved
in the disorder. The volume status can sometimes be determined
on a clinical basis and can be aided by simple plasma and urine
electrolytes.
16. SIADH
• While inappropriate AVP secretion
can occur with any cancer, it is most
frequently reported with small-cell
lung cancer, head and neck
carcinomas, hematologic
malignancies, and non–small-cell
lung cancer.
• Drugs reported to cause SIADH
include cyclophosphamide and its
isomeric analogue, ifosfamide; the
vinca alkaloids including vincristine,
vinblastine, and vinorelbine; the
proteasome inhibitor bortezomib;
as well as carboplatin and
cisplatin, although the later more
frequently cause renal salt wasting.
17. • Patients with small-cell lung cancer, hyponatremia, and without
measurable AVP have also been reported. In a fraction of these
patients, ectopic production of ANP mRNA and a peptide similar to
the bioactive 28-amino acid ANP form present in plasma has been
shown in tumors and leads to hyponatremia.
• Normally, ANP is produced, stored, and released by atrial myocytes
and binds to a specific set of receptors increasing renal sodium
excretion.
18. Besides SIADH and syndrome of inappropriate atrial natriuretic
peptide (SIANP) production, there is increasing awareness of an
alternate mechanism of salt loss referred to as cerebral salt wasting
syndrome (CSWS).
Two major criteria must be met for a diagnosis of CSWS:
1) a cerebral lesion and
2) high urinary excretion of Na+ and Cl– , in a patient with
contraction of the extracellular fluid volume.
While the frequency of CSWS is less, it is important to make the
correct diagnosis as management is different
1. Aggressive fluid and electrolyte replacement
2. Mineralocorticoid supplementation (fludrocortisone 100–400 mg/d)
19. The acuity of onset of hyponatremia predicts for the risk of
complications, and identifying patients with an acute drop
in sodium levels (<48 hours) is probably the most important factor in
determining treatment.
In patients with chronic hyponatremia, there is a higher risk of
complications of overaggressive treatment, and it is probably in these
patients that vasopressin antagonists tolvaptan and conivaptan should
be used in an outpatient setting.
20. • High-risk individuals include those with a serum sodium level of <105
mmol/L, heavy alcohol intake, advanced liver disease, hypokalemia,
and malnutrition.
• Although the risk of mortality is increased with all degrees of
hyponatremia, deaths from neurologic complications including
cerebral edema and osmotic demyelination are rare.
23. GENERALGUIDELINES
• Na deficit = 0.6 x wt(kg) x (desired [Na] - actual [Na])
• When do we need to Rx quickly?
• Acute (<24h) severe (< 120 mEq/L) Hyponatremia
• Prevent brain swelling or Rx brain swelling
• Symptomatic Hyponatremia (Seizures, coma, etc.)
• Alleviate symptoms
• Initially treat “Quickly”: 3% NS, 1 mEq/kg/h until:
• Symptoms stop
• 3-4h elapsed and/or Serum Na has reached 120 mEq/L
• Then 0.5 mEq/L/h with 0.9% NS or simply fluid restriction.
• Aim for overall 24h correction to be < 10-12 mEq/L/d to prevent myelinolysis
24. • Acute Hypo-natremia with severe Neurological symptoms(headache,
nausea, and/or vomiting, seizures, obtundation , and central
herniation)
• Rate of plasma Sodium correction should be 0.5 -2 mEq/L/Hr for the
first 3-4 hrs or severe neurological symptom improves.
• <10-12 mEq /24Hr.
25. • Chronic asymptomatic Hyponatremia
-Rate of plasma Sodium correction should be
-< 0.5 to 1.0 mEq/L/Hr
-On first day < 10-12 mEq/L
-On First Two day < 18 mEq/L
->25 mEq/48 hrs or Until normo-natremia is at risk of ODS.
• Stop non-essential fluids, medications.
• Cause-specific treatment.
• Fluid restriction.
27. Example -
• A 30kgs girl with serum sodium of 110meq/L
• Total body water = 30kgs * 0.5 = 15
• Change in serum sodium
• = infusate Na – serum Na / (Total body water+1)
• = 513 -110 / ( 15+1)
• = 25.18 meq/L
28. • So from the above equation – 25meq is corrected by
1Litre of 3% NaCl.
• But we need to correct Na by 10-12 meq in first 24hrs .
• So around 400ml of 3% NaCl will correct around 10meq.
• 400ml of 3% NaCl should be given in 24hrs and this can
be given @16ml/hr.
29. SIADH
• Severe hypo-natremia with
hypertonic saline.
• Fluid restriction- 0.5- 1 Lt per
day.
• Demeclocycline.
• Vaptans.
30. Tolvaptan has been studied in a small trial involving cancer patients
with hyponatremia. However, despite a superiority in correcting sodium
levels, there was no difference in mortality or length of stay. Therefore,
because of the expense of this agent, the use of vasopressin
antagonists has not been recommended yet for inpatient use.
• Care should be taken with sodium replacement and the treatment of
other forms of hyponatremia to not correct extremely low sodium
levels too rapidly because of the risk of osmotic demyelination.
• Osmotic demyelination can be avoided by correcting sodium at a rate
that does not exceed 8 mEq/L per day and, in high-risk patients, 4 to
6 mEq/L per day.
31. HYPERNATREMIA
• Hypernatremia is defined as an increase in the plasma
Na+ concentration to >145 m M .
• Mortality rates of as high as 40–60%
• Hypernatremia is usually the result of a combined water
and electrolyte deficit, with losses of H2O in excess of
Na+.
• Less frequently, the ingestion or iatrogenic administration
of excess Na+ can be causative, for example after IV
administration of excessive hypertonic Na+-Cl– or Na+-
HCO3–
36. Example-
• 30kgs girl with 168 Sodium.
• Total body water – 30kgs * 0.5 = 15
• We will use 5% Dextrose solution for correction in this
patient.
• Change in serum sodium
= infusate Na – serum Na / (Total body water+1)
= 0-168 / (15 +1)
= -10.5
37. • So Change in serum Na by 1 litre of 5% Dextrose
solution is 10.5meq/L.
• We need to correct serum sodium by 10-12meq/L in
24hours.
• So we will give 1litre of 5% Dextrose solution in 24hours
– which can be given @40ml/hr.
38. Alternate Method
• First, calculate water deficit
• Water deficit =CBW X wt X ((plasma Na/desired Na level)-1)
• CBW = current body water assumed to be 60% of body
weight in men and 50% in women
• So let’s do a sample calculation:
• 30 kg girl with 168 mEq/L
• How much water will it take to reduce her sodium to 140 mEq/L
39. Calculation continued-
• Water deficit = 0.5x 30 ([168/140]-1} = 3 L
• But how fast should I correct it?
• Same as hyponatremia, sodium should not be lowered by
more than 10-12 mEq/L in 24 hours
• Overcorrection can lead to cerebral edema which can
lead to encephalopathy, seizures or death
• So what does that mean for our patient?
• The 3L which will lower the sodium level by 28 should
be given over 56-60 hours, or at a rate of 75-80 mL/hr
• Typical fluids given in form of D5 water.
41. Hypercalcemia
Incidence, Etiology, and Diagnosis
• Hypercalcemia is also a common problem in cancer patients,
occurring in 20% to 30% of all cancer patients at some point in their
disease course.
• The finding of hypercalcemia in a cancer patient often confers a poor
prognosis, with one series finding that most patients died within 30
days.
• The constellation of symptoms is well known to all students of
medicine who have learned the well-known mnemonic “stones,
bones, moans, abdominal groans, and psychiatric overtones.”
(nausea, vomiting, constipation, polyuria, and disorientation).
42. • Hypercalcemia can be divided into the following four types:
• 1. Local osteolytic hypercalcemia
• 2. Humoral hypercalcemia of malignancy (secretion of parathyroid
hormone–related peptide) –(MC- 80%)
• 3. 1,25-Dihydroxyvitamin D–secreting lymphomas
• 4. Ectopic hyperparathyroidism
• The main principles of treatment of hypercalcemia are targeting the
underlying malignancy, correction of dehydration with aggressive fluid
resuscitation, and prevention of bone resorption with
bisphosphonates and rank ligand inhibition.
46. It is usually best to categorize hypercalcemia patients into two groups: those
who can be treated less aggressively in an outpatient setting and those who
need hospitalization.
47. Management
• Therapeutic interventions depend on the presentation.
• Asymptomatic patients with a serum calcium level of ≤3.25 mmol/L
can be managed conservatively, whereas symptomatic patients or
those with a serum calcium level >3.25 mmol/L require immediate
aggressive measures.
• Although hydration results at most in only a mild (0.5 mmol/L [∼2
mg/dL]) decrease in serum calcium levels, it is a simple, rapid, and
effective intervention that can also preclude continued renal calcium
reabsorption.
• After adequate hydration, 20 to 40 mg of intravenous furosemide can
enhance calcium excretion.
• Together with hydration, bisphosphonates are the cornerstone of
therapy for malignancy-associated hypercalcemia.
48. • Bisphosphonates are based on a phosphorous-carbon-phosphorous
backbone, similar to pyrophosphate. The carbon replacing the central
oxygen renders the molecules resistant to hydrolysis, but allows the
retention of pyrophosphate-like inhibition of bone resorption. Their
mechanism of action is complex.
• Evidence indicates non– nitrogen-containing bisphosphonates such
as clodronate resemble pyrophosphate and are metabolized
intracellularly to nonhydrolyzable analogues of ATP that inhibit ATP-
dependent intracellular enzymes and are thus cytotoxic.
• Nitrogen-containing bisphosphonates (aminobisphosphonates),
including pamidronate, ibandronate, and zoledronate, impede protein
prenylation and bone resorption by osteoclasts by inhibiting the
mevalonate pathway (farnesyl diphosphate synthase) disrupting the
signaling functions of key regulatory proteins.
49. • Bisphosphonates have an onset of action of approximately 48hours
and a nadir in calcium levels of 5 to 7 days. Zoledronic acid, the
preferred agent, is given at a dose of 4 mg over 15 minutes and has
been shown to be superior to pamidronate. The average duration of
response is 32 days .
• Bisphosphonates are most effective in the therapy of hypercalcemia
associated with multiple myeloma, but are also efficacious in solid
tumors with skeletal metastases. They are somewhat less effective in
the treatment of patients with humoral-mediated hypercalcemia
because they have no effect on tubular calcium reabsorption
mediated by humoral factors, including PTHrP.
50. • Zolendronic acid can be given weekly for patients with persistent
hypercalcemia. It is a well-tolerated agent, but adverse events of mild
nephrotoxicity, flu-like syndrome, musculoskeletal pain, and
hypocalcemia have been reported. Osteonecrosis of the jaw is a
chronic side effect occurring in about 1% to 2% of patients.
• Calcitonin has the advantage of acting rapidly in 6 to 24 hours,can
be given prior to hydration, and is not nephrotoxic. However, it
exhibits rapid tachyphylaxis and can only be given for two doses.
Therefore, it should be used in severe hypercalcemia or in cases of
renal failure. Other agents such as gallium nitrate are rarely used
today.
51. • Osteoprotegerin (OPG) is a naturally occurring soluble receptor that
inhibits bone resorption by inhibiting osteoclast differentiation.
• OPG is part of a cytokine system that belongs to the tumor necrosis
factor superfamily. The components include the ligand RANKL
(receptor activator of nuclear factor-κΒ ligand), its specific receptor
RANK (receptor activator of nuclear factor-κΒ) and OPG, a soluble
“decoy” receptor.
• By binding to RANK, RANKL enhances bone resorption by
(1) increasing osteoclast formation from hematopoietic precursors,
(2) increasing osteoclast activity, and
(3) inhibiting osteoclast apoptosis.
• By acting as a “decoy,” intravenous administration of OPG has potent
hypocalcemic effects in murine models of humoral hypercalcemia.
52. • Denosumab, a fully human monoclonal antibody with a high affinity
and specificity for RANKL, is approved by the US Food and Drug
Administration “for prevention of skeletal-related events in patients
with bone metastases from solid tumors . . . but is not indicated for the
prevention of skeletal-related events in patients with multiple
myeloma.”
• Repeated doses of denosumab, 120 mg given subcutaneously, may
be effective in patients with hypercalcemia of malignancy who have
lost responsiveness to bisphosphonates.
53.
54. • Mild hypercalcemia (≤3 mmol/L [12 mg/dL)]) can usually be managed
by hydration.
• Severe hypercalcemia (≥3.7 mmol/L [15 mg/dL]) requires rapid
correction. IV pamidronate, or zolendronate, or subcutaneous
denosumab should be administered. In addition, for the first 24–48 h,
aggressive sodium-calcium diuresis with IV saline should be given
and, following rehydration, large doses of furosemide or ethacrynic
acid, but only if appropriate monitoring is available and cardiac and
renal function are adequate.
• Intermediate degrees of hypercalcemia between 3 and 3.7 mmol/L
(12 and 15 mg/dL) should be approached with vigorous hydration and
then the most appropriate selection for the patient of the combinations
used with severe hypercalcemia.
56. Lactic acidosis
• Lactic acidosis is defined as a pH ≤7.35 with plasma lactate
concentration ≥5 mEq/L. It has been reported more frequently as a
complication of hematologic malignancies but can be a rare event in
solid tumors, often associated with liver metastases.
• Often, the acidosis is associated with an elevated anion gap, but in
cancer patients with poor nutrition and low albumin levels, the anion
gap may not be appropriately corrected.
• Lactic acidosis occurs when the production of lactate exceeds the
ability metabolize it. Overproduction is a result of circulatory,
respiratory, hematologic, or cellular dysfunction or collapse, whereas
underutilization can be a result of poor hepatic perfusion.
57. • Lactate is generated largely by anaerobic glycolysis (Embden-
Meyerhof-Parnas pathway).
• Cancer cells produce energy primarily through glycolysis because of
oncogene-driven metabolic reprogramming designed to promote
cancer cell survival (Warburg effect).
• Although cancer can result in lactic acidosis by itself, other serious
causes may also be present and will need to be concurrently
managed aggressively, including shock, heart failure, sepsis, hypoxia,
anemia, and various medication side effects
• Bicarbonate infusions are sometimes used as a temporary measure
to reverse acidemia, especially in patients with malignancies where
the underlying cause may not be rapidly reversible. In the absence of
proven outcomes data , however, such infusions should be used
judiciously.
60. Hyperammonemia
Incidence, Etiology, and Diagnosis
• Cancer and its treatments can be causes of hyperammonemia and
hepatic encephalopathy. This represents an impairment of the mental
state because of impaired hepatic function and accumulation of
ammonia from the gut.
• The detailed pathogenesis and array of symptoms are varied and
complex, but in cancer patients, disorder of the blood–brain barrier
may be an important factor.
• Although the symptoms can be varied, severe findings such as
asterixis, confusion, somnolence, and coma define states requiring
emergent intervention.
61. • Patients suspected of having hepatic encephalopathy should also be
checked for other reversible causes including hypoxia, hypercapnia,
acidosis, uremia, medications (including rare side effects of novel
agents), electrolyte abnormalities, central nervous system metastases
or hemorrhage, and hypoglycemia.
• Serial measurements of ammonia levels are generally not
recommended during treatment because they often lag behind clinical
response. Because most patients show an improvement in clinical
symptoms within 48 hours of initiation of therapy, those who donot
recover should be evaluated for one of the differential causes listed
previously.
63. • Patients who do not respond rapidly may need to be moved to a more
intensive care setting and require the assistance of hepatologists or
transplant teams. Medications such as rifaximin and neomycin can be
considered in refractory cases.
• Aggressive treatment of hypokalemia is important because this will
reduce renal production of ammonia. who do not recover should be
evaluated for one of the differential causes listed previously.