There are three major acute complications of diabetes related to short-term imbalances in blood glucose levels: hypoglycemia, diabetic ketoacidosis (DKA), and hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Hypoglycemia occurs when blood glucose levels fall below normal ranges and can cause symptoms ranging from mild to severe depending on severity. DKA is caused by a lack of insulin and results in high blood glucose, dehydration, and acidosis. HHNS involves very high blood glucose without acidosis due to relative insulin deficiency and dehydration from inadequate fluid intake. Both DKA and HHNS are medical emergencies treated by fluid replacement, electrolyte management, and insulin
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
The endocrine pancreas
Islets of Langerhans (endocrine pancreas) contain 4 major
and 2 minor cell types.
●Major cell types:
1.β cell produces insulin.
2.α cell secretes glucagon.
3.δ cells contain somatostatin, which suppresses
both insulin and glucagon release.
• DM is a heterogeneous group of syndromes characterized by
an elevation of fasting blood glucose caused by absolute or
relative deficiency of insulin
• Hyperglycemia in diabetes results from defects in insulin
secretion ( destruction of β cells of the pancreas ), insulin
action, or most commonly both.
• Diabetes is the leading cause of adult blindness and
amputation and a major cause of renal failure, nerve damage,
heart attacks, and strokes.
• Most cases of diabetes mellitus can be separated into two
groups
- Type 1 (insulin-dependent DM)
- Type 2 (noninsulin dependent DM)
Type 1 Diabetes Mellitus
• Onset: usually during childhood
• Caused by absolute (complete) deficiency of insulin:
- Maybe caused by both:
1. autoimmune attack of b-cells of the pancreas, i.e. a
genetic determinant that allows the β cells to be
recognized as “nonself”
2. environmental factors as viral infection or toxins
• Rapid symptoms appear when 80-90% of the b-cells
have been destroyed
• Commonly complicated by diabetic ketoacidosis (DKA)
• Treated only by insulin
• the islets of Langerhans become
infiltrated with activated T
lymphocytes, leading to a
condition called insulitis .
• Over a period of years, this
autoimmune attack on the β cells
leads to gradual depletion of the
β-cell population. However,
symptoms appear abruptly when
80%–90% of the β cells have been
destroyed.
• At this point, the pancreas fails to
respond adequately to ingestion
of glucose, and insulin therapy is
required to restore metabolic
control and prevent lifethreatening ketoacidosis.
Metabolic changes of type 1 DM
1-Hyperglycemia: increased glucose in blood, Due to:
Decreased glucose uptake by muscles & adipose tissues &/or
Increased hepatic gluconeogenesis
2-Ketoacidosis:
• increased ketone bodies in blood (in untreated or
uncontrolled cases) results from increased mobilization of
fatty acids (FAs ) from adipose tissue, combined with
accelerated hepatic FA β-oxidation and synthesis of 3-
hydroxybutyrate and acetoacetate.
• in 25 – 40% of newly diagnosed type 1 DM
• in stress states demanding more insulin (as during
infection, illness or during surgery)
• In patients who have no compliance with therapy
3- Hypertriglyceridemia: increased TAG in blood
• Released fatty acids from adipose tissues are
converted to triacylglycerol. Triacylglycerol is
secreted from the liver in VLDL to blood.
• Chylomicrons (from diet fat) accumulates (low
lipoprotein lipase in DM due to decreased
insulin)
• Increased VLDL & chylomicrons results in
hypertriacylglyceridemia
INTERTISSUE RELATIONSHIP IN T1DM
Diagnosis of type 1 DM
• Clinically:
Age: during childhood or puberty (< 20 years of age)
- Polyuria (frequent urina
The endocrine pancreas
Islets of Langerhans (endocrine pancreas) contain 4 major
and 2 minor cell types.
●Major cell types:
1.β cell produces insulin.
2.α cell secretes glucagon.
3.δ cells contain somatostatin, which suppresses
both insulin and glucagon release.
• DM is a heterogeneous group of syndromes characterized by
an elevation of fasting blood glucose caused by absolute or
relative deficiency of insulin
• Hyperglycemia in diabetes results from defects in insulin
secretion ( destruction of β cells of the pancreas ), insulin
action, or most commonly both.
• Diabetes is the leading cause of adult blindness and
amputation and a major cause of renal failure, nerve damage,
heart attacks, and strokes.
• Most cases of diabetes mellitus can be separated into two
groups
- Type 1 (insulin-dependent DM)
- Type 2 (noninsulin dependent DM)
Type 1 Diabetes Mellitus
• Onset: usually during childhood
• Caused by absolute (complete) deficiency of insulin:
- Maybe caused by both:
1. autoimmune attack of b-cells of the pancreas, i.e. a
genetic determinant that allows the β cells to be
recognized as “nonself”
2. environmental factors as viral infection or toxins
• Rapid symptoms appear when 80-90% of the b-cells
have been destroyed
• Commonly complicated by diabetic ketoacidosis (DKA)
• Treated only by insulin
• the islets of Langerhans become
infiltrated with activated T
lymphocytes, leading to a
condition called insulitis .
• Over a period of years, this
autoimmune attack on the β cells
leads to gradual depletion of the
β-cell population. However,
symptoms appear abruptly when
80%–90% of the β cells have been
destroyed.
• At this point, the pancreas fails to
respond adequately to ingestion
of glucose, and insulin therapy is
required to restore metabolic
control and prevent lifethreatening ketoacidosis.
Metabolic changes of type 1 DM
1-Hyperglycemia: increased glucose in blood, Due to:
Decreased glucose uptake by muscles & adipose tissues &/or
Increased hepatic gluconeogenesis
2-Ketoacidosis:
• increased ketone bodies in blood (in untreated or
uncontrolled cases) results from increased mobilization of
fatty acids (FAs ) from adipose tissue, combined with
accelerated hepatic FA β-oxidation and synthesis of 3-
hydroxybutyrate and acetoacetate.
• in 25 – 40% of newly diagnosed type 1 DM
• in stress states demanding more insulin (as during
infection, illness or during surgery)
• In patients who have no compliance with therapy
3- Hypertriglyceridemia: increased TAG in blood
• Released fatty acids from adipose tissues are
converted to triacylglycerol. Triacylglycerol is
secreted from the liver in VLDL to blood.
• Chylomicrons (from diet fat) accumulates (low
lipoprotein lipase in DM due to decreased
insulin)
• Increased VLDL & chylomicrons results in
hypertriacylglyceridemia
INTERTISSUE RELATIONSHIP IN T1DM
Diagnosis of type 1 DM
• Clinically:
Age: during childhood or puberty (< 20 years of age)
- Polyuria (frequent urina
Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
Empowering ACOs: Leveraging Quality Management Tools for MIPS and BeyondHealth Catalyst
Join us as we delve into the crucial realm of quality reporting for MSSP (Medicare Shared Savings Program) Accountable Care Organizations (ACOs).
In this session, we will explore how a robust quality management solution can empower your organization to meet regulatory requirements and improve processes for MIPS reporting and internal quality programs. Learn how our MeasureAble application enables compliance and fosters continuous improvement.
Medical Technology Tackles New Health Care Demand - Research Report - March 2...pchutichetpong
M Capital Group (“MCG”) predicts that with, against, despite, and even without the global pandemic, the medical technology (MedTech) industry shows signs of continuous healthy growth, driven by smaller, faster, and cheaper devices, growing demand for home-based applications, technological innovation, strategic acquisitions, investments, and SPAC listings. MCG predicts that this should reflects itself in annual growth of over 6%, well beyond 2028.
According to Chris Mouchabhani, Managing Partner at M Capital Group, “Despite all economic scenarios that one may consider, beyond overall economic shocks, medical technology should remain one of the most promising and robust sectors over the short to medium term and well beyond 2028.”
There is a movement towards home-based care for the elderly, next generation scanning and MRI devices, wearable technology, artificial intelligence incorporation, and online connectivity. Experts also see a focus on predictive, preventive, personalized, participatory, and precision medicine, with rising levels of integration of home care and technological innovation.
The average cost of treatment has been rising across the board, creating additional financial burdens to governments, healthcare providers and insurance companies. According to MCG, cost-per-inpatient-stay in the United States alone rose on average annually by over 13% between 2014 to 2021, leading MedTech to focus research efforts on optimized medical equipment at lower price points, whilst emphasizing portability and ease of use. Namely, 46% of the 1,008 medical technology companies in the 2021 MedTech Innovator (“MTI”) database are focusing on prevention, wellness, detection, or diagnosis, signaling a clear push for preventive care to also tackle costs.
In addition, there has also been a lasting impact on consumer and medical demand for home care, supported by the pandemic. Lockdowns, closure of care facilities, and healthcare systems subjected to capacity pressure, accelerated demand away from traditional inpatient care. Now, outpatient care solutions are driving industry production, with nearly 70% of recent diagnostics start-up companies producing products in areas such as ambulatory clinics, at-home care, and self-administered diagnostics.
CHAPTER 1 SEMESTER V PREVENTIVE-PEDIATRICS.pdfSachin Sharma
This content provides an overview of preventive pediatrics. It defines preventive pediatrics as preventing disease and promoting children's physical, mental, and social well-being to achieve positive health. It discusses antenatal, postnatal, and social preventive pediatrics. It also covers various child health programs like immunization, breastfeeding, ICDS, and the roles of organizations like WHO, UNICEF, and nurses in preventive pediatrics.
Global launch of the Healthy Ageing and Prevention Index 2nd wave – alongside...ILC- UK
The Healthy Ageing and Prevention Index is an online tool created by ILC that ranks countries on six metrics including, life span, health span, work span, income, environmental performance, and happiness. The Index helps us understand how well countries have adapted to longevity and inform decision makers on what must be done to maximise the economic benefits that comes with living well for longer.
Alongside the 77th World Health Assembly in Geneva on 28 May 2024, we launched the second version of our Index, allowing us to track progress and give new insights into what needs to be done to keep populations healthier for longer.
The speakers included:
Professor Orazio Schillaci, Minister of Health, Italy
Dr Hans Groth, Chairman of the Board, World Demographic & Ageing Forum
Professor Ilona Kickbusch, Founder and Chair, Global Health Centre, Geneva Graduate Institute and co-chair, World Health Summit Council
Dr Natasha Azzopardi Muscat, Director, Country Health Policies and Systems Division, World Health Organisation EURO
Dr Marta Lomazzi, Executive Manager, World Federation of Public Health Associations
Dr Shyam Bishen, Head, Centre for Health and Healthcare and Member of the Executive Committee, World Economic Forum
Dr Karin Tegmark Wisell, Director General, Public Health Agency of Sweden
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptxR3 Stem Cell
R3 Stem Cells and Kidney Repair: A New Horizon in Nephrology" explores groundbreaking advancements in the use of R3 stem cells for kidney disease treatment. This insightful piece delves into the potential of these cells to regenerate damaged kidney tissue, offering new hope for patients and reshaping the future of nephrology.
Health Education on prevention of hypertensionRadhika kulvi
Hypertension is a chronic condition of concern due to its role in the causation of coronary heart diseases. Hypertension is a worldwide epidemic and important risk factor for coronary artery disease, stroke and renal diseases. Blood pressure is the force exerted by the blood against the walls of the blood vessels and is sufficient to maintain tissue perfusion during activity and rest. Hypertension is sustained elevation of BP. In adults, HTN exists when systolic blood pressure is equal to or greater than 140mmHg or diastolic BP is equal to or greater than 90mmHg. The
Explore our infographic on 'Essential Metrics for Palliative Care Management' which highlights key performance indicators crucial for enhancing the quality and efficiency of palliative care services.
This visual guide breaks down important metrics across four categories: Patient-Centered Metrics, Care Efficiency Metrics, Quality of Life Metrics, and Staff Metrics. Each section is designed to help healthcare professionals monitor and improve care delivery for patients facing serious illnesses. Understand how to implement these metrics in your palliative care practices for better outcomes and higher satisfaction levels.
Telehealth Psychology Building Trust with Clients.pptxThe Harvest Clinic
Telehealth psychology is a digital approach that offers psychological services and mental health care to clients remotely, using technologies like video conferencing, phone calls, text messaging, and mobile apps for communication.
One of the most developed cities of India, the city of Chennai is the capital of Tamilnadu and many people from different parts of India come here to earn their bread and butter. Being a metropolitan, the city is filled with towering building and beaches but the sad part as with almost every Indian city
CHAPTER 1 SEMESTER V - ROLE OF PEADIATRIC NURSE.pdfSachin Sharma
Pediatric nurses play a vital role in the health and well-being of children. Their responsibilities are wide-ranging, and their objectives can be categorized into several key areas:
1. Direct Patient Care:
Objective: Provide comprehensive and compassionate care to infants, children, and adolescents in various healthcare settings (hospitals, clinics, etc.).
This includes tasks like:
Monitoring vital signs and physical condition.
Administering medications and treatments.
Performing procedures as directed by doctors.
Assisting with daily living activities (bathing, feeding).
Providing emotional support and pain management.
2. Health Promotion and Education:
Objective: Promote healthy behaviors and educate children, families, and communities about preventive healthcare.
This includes tasks like:
Administering vaccinations.
Providing education on nutrition, hygiene, and development.
Offering breastfeeding and childbirth support.
Counseling families on safety and injury prevention.
3. Collaboration and Advocacy:
Objective: Collaborate effectively with doctors, social workers, therapists, and other healthcare professionals to ensure coordinated care for children.
Objective: Advocate for the rights and best interests of their patients, especially when children cannot speak for themselves.
This includes tasks like:
Communicating effectively with healthcare teams.
Identifying and addressing potential risks to child welfare.
Educating families about their child's condition and treatment options.
4. Professional Development and Research:
Objective: Stay up-to-date on the latest advancements in pediatric healthcare through continuing education and research.
Objective: Contribute to improving the quality of care for children by participating in research initiatives.
This includes tasks like:
Attending workshops and conferences on pediatric nursing.
Participating in clinical trials related to child health.
Implementing evidence-based practices into their daily routines.
By fulfilling these objectives, pediatric nurses play a crucial role in ensuring the optimal health and well-being of children throughout all stages of their development.
CHAPTER 1 SEMESTER V - ROLE OF PEADIATRIC NURSE.pdf
Gada DM 2022 Modfied_1401-5-18-14-46.pptx
1. Acute Complications of Diabetes
There are three major acute complications of diabetes related to
short-term imbalances in blood glucose levels:
a. Hypoglycemia
b. Diabetic ketoacidosis/DKA, and
c. Hyperglycemic hyperosmolar non ketotic syndrome/HHNS, which
is also called hyperglycemic hyperosmolar syndrome or state
2. Hypoglycemia (Insulin Reactions)
Occurs when the BGLs falls to < 50 to 60mg/dL (2.7 to
3.3mmol/L)
Causes
Too much insulin or OHAs
Too little food
Excessive physical activity
Often occurs before meals, especially if meals are delayed or
snacks are omitted
3. Hypoglycemia Clinical manifestations
i. Mild hypoglycemia
Stimulation of sympathetic nervous system resulting in a surge of
epinephrine and norepinephrine
In turn results in:
Sweating
Tremor
Tachycardia
Palpitation
Nervousness
Hunger
4. Hypoglycemia C/Ms Cont’d
ii. Moderate hypoglycemia
Drop in BGL deprives the brain cells of needed fuel for
functioning
Signs of impaired function of the CNS may include:
Inability to concentrate
Head ache, Light headiness,
Confusion, Memory loses,
Slurred speech,
Double vision
Drowsiness,
Numbness of the lips and tongue
5. Hypoglycemia C/Ms Cont’d
Sever hypoglycemia
Results in:
Impaired CNS functions
Disoriented behavior
Seizures,
Difficulty arousing from sleep, and
Loss of consciousness
6. Management
A. Immediate treatment with carbohydrate
The usual recommendation is for 15 g of a fast-acting concentrated
source of carbohydrate such as the following, given orally:
A. Three or four commercially prepared glucose tablets
B.100-150 ml of fruit juice or regular soda
C.6 to 10 hard candies
D.2 to 3 teaspoons of sugar or honey
Nursing Alert: To prevent sharp increase in BGL, it is not
necessary to add sugar to juice, even if it is labeled as unsweetened
juice: the fruit sugar in juice contains enough carbohydrate to raise
the BGL
7. Management Immediate treatment with carbohydrate…
The BGL should be retested in 15 minutes and retreated if it is
less than 70 to 75 mg/dL (3.8 to 4 mmol/L)
If the symptoms persist for longer than 10 to 15 minutes after
initial treatment, the treatment is repeated
Once the symptoms resolve, a snack containing protein and
starch (eg, milk or cheese and bananas/crackers) is recommended
unless the patient plans to eat a regular meal or snack within 30 to
60 minutes
8. Management Immediate treatment with carbohydrate…
B. Initiating Emergency Measures
Glucagon injection:
Has an onset of 8 to 10 minutes, and its action lasts 12 to 27 minutes
For adults who are unconscious and cannot swallow, an injection of
glucagon 1mg can be administered either subcutaneously or
intramuscularly
After injection of glucagon, the patient may take as long as 20
minutes to regain consciousness
9. Management Immediate treatment with carbohydrate…
A concentrated source of carbohydrate:
Should be given to the patient on awakening to prevent recurrence of
hypoglycemia followed by a snack
50%/40% Dextrose in water (D50W/D40W)
For patients who are unconscious or cannot swallow
25 to 50 mL of 50%/40% dextrose in water may be administered IV
The effect is usually seen within minutes
10. Cont…
Providing Patient Education
Consistent pattern of eating, administering insulin, and exercising
Between-meal and bedtime snacks may be needed to counteract the
maximum insulin effect
The patient should cover the time of peak activity of insulin by eating
a snack and by taking additional food when physical activity is
increased
Routine blood glucose tests to anticipate change insulin requirements
and to adjust the dosage
11. Cont…
To prevent unexpected hypoglycemia all patients treated with
insulin should wear an identification bracelet or tag stating that
they have diabetes Symptoms of hypoglycemia
Patients with diabetes, especially those receiving insulin, learn to
carry some form of simple sugar with them at all times
Advising to refrain from eating high-calorie, high-fat dessert
foods (eg, cookies, cakes, ice cream) to treat hypoglycemia
because their high fat content may slow the absorption of the
glucose and resolution of the hypoglycemic symptoms
12. Diabetic Ketoacidosis (DKA)
Diabetic Ketoacidosis (DKA)
Definition
DKA is a metabolic derangement in T1D that is caused by an
absence or markedly inadequate amount of insulin
Insulin deficiency results in disorders in the metabolism of
carbohydrate, protein, and fat
13. DKA Causes: Three main causes
1. Decreased or missed dose or deficiency of insulin caused by:
An insufficient dosage of insulin prescribed
An insufficient insulin being administered by the patient
Patient error in drawing up or injecting insulin
Intentional skipping of insulin doses
Equipment problems
2. Illness or infection
3. Undiagnosed and untreated diabetes
14. DKA Causes …
Illnesses and infections are associated with insulin resistance
In response to physical (and emotional) stressors, there is an
increase in the level of “stress” hormones:
Glucagon,
Epinephrine, norepinephrine,
Cortisol, and
Growth hormone
These hormones promote glucose production by the liver and
interfere with glucose utilization by muscle and fat tissue
15. DKA: Pathophysiology
The three main clinical features of DKA are:
1.Hyperglycemia
2.Dehydration and electrolyte loss
3.Acidosis
16. Pathophysiology DKA
DKA results from relative or absolute insulin deficiency combined
with counter regulatory hormone excess (glucagon,
catecholamine's, cortisol, and growth hormone).
Both insulin deficiency and glucagon excess, in particular, are
necessary for DKA to develop.
The decreased ratio of insulin to glucagon promotes
gluconeogenesis, glycogenolysis, and ketone body formation in the
liver, as well as increases in substrate delivery from fat and muscle
(free fatty acids, amino acids) to the liver.
Markers of inflammation (cytokines, C-reactive protein) are
elevated in both DKA and HHS
The combination of insulin deficiency and hyperglycemia reduces
the hepatic level of fructose-2,6-bisphosphate, which alters the
activity of phosphofructokinase and fructose-1,6-bisphosphatase.
17. release of free fatty acids. Normally, these free fatty acids are
converted to triglycerides or very-low-density lipoprotein
(VLDL) in the liver.
However, in DKA, hyper glucagonemia alters hepatic
metabolism
to favor ketone body formation, through activation of the enzyme
carnitine palmitoyltransferase I.
This enzyme is crucial for regulating fatty acid transport into the
mitochondria, where beta oxidation and conversion to ketone
bodies occur. At physiologic pH, ketone bodies
exist as ketoacids, which are neutralized by bicarbonate.
As bicarbonate stores are depleted, metabolic acidosis ensues.
Increased lactic acid production also contributes to the acidosis.
18. DKA: Diagnosis
BGLs may vary from 300 to 800mg /dL
Serum Bicarbonate 0-15mq/L
PH 6.8-7.3
PaCO2 10-30mmHg – Respiratory compensation
Increased creatinine
Increased BUN
Increased hematocrite
19. DKA: Prevention
If DKA is related to illness, teach the patient about “Sick
day” rules for managing their diabetes when ill
Assess diabetic self management skills including blood
glucose testing and insulin administration
If insulin dose is intentionally altered, psychological
counseling is recommended for patients and family
members
20. Cont…
1.Take insulin or oral antidiabetic agents as usual.
2.Test blood glucose and test urine ketones every 3 to 4 h.
3.Report elevated glucose levels (300 mg/dL [16.6 mmol/L] or as
otherwise specified) or urine ketones to your health care provider.
4.If you take insulin, you may need supplemental doses of regular insulin
every 3 to 4 h.
5.If you cannot follow your usual meal plan, substitute soft foods (eg, 1
cup cream soup, 1⁄2 cup custard, 3 squares graham bananas) six to eight
times per day
21. DKA Prevention: “Sick Day Rules”…
6.If vomiting, diarrhea, or fever persists, take liquids (eg, 1⁄2 cup
regular cola or orange juice, 1⁄2 cup broth, 1 cup Gatorade) every
1⁄2 to 1 hour to prevent dehydration and to provide calories.
7.Report nausea, vomiting, and diarrhea to your health care
provider, because extreme fluid loss may be dangerous.
8.If you are unable to retain oral fluids, you may require
hospitalization to avoid diabetic ketoacidosis and possibly coma
24. Hyperglycemic hyperosmolar…
Hyperglycemic hyperosmolar state(HHS) is a hyperglycemic
emregncy that occurs in type 2 DM due to relative insulin
deficiency and inadequate fluid intake.
Occurs most often in older people (50 to 70 years of age) who
have no known history of diabetes or who have type 2 diabetes
Except the acidosis the manifesations, risk factors and
management of HHS is similar to DKA
25. Cont…
Hyper osmolality and hyperglycemia are predominant
The patient’s persistent hyperglycemia causes osmotic diuresis,
resulting in losses of water and electrolytes.
Because of water shifts from ICF space to ECF space the patient
may present with neurologic abnormalities such as:
Somnolence, coma,
Seizures,
Hemiparesis, and
Aphasia
26. Cont…
HHNS: Precipitating factors
i. Acute illness (e.g. pneumonia, stroke)
ii. Medications that exacerbate BGL (e.g. thiazides)
iii. Treatments such as dialysis
27. Pathophysiology HHS
Relative insulin deficiency and inadequate fluid
intake are the underlying causes of HHS.
Insulin deficiency increases hepatic glucose production (through glycogenolysis
and gluconeogenesis) and impairs glucose utilization in skeletal muscle (see
above
discussion of DKA).
Hyperglycemia induces an osmotic diuresis that leads to intravascular volume
depletion, which is exacerbated by
inadequate fluid replacement. The absence of ketosis in HHS is not
understood.
Presumably, the insulin deficiency is only relative and less
severe than in DKA.
Lower levels of counter regulatory hormones and
free fatty acids have been found in HHS than in DKA in some studies.
It is also possible that the liver is less capable of ketone body synthesis
or that the insulin/glucagon ratio does not favor ketogenesis.
28. Laboratory Abnormalities and Diagnosis
The laboratory features in HHS
Most notable are the marked hyperglycemia (plasma glucose may
be >55.5 mmol/L [1000 mg/dL]), hyperosmolality (>350
mosmol/L), and prerenal azotemia.
The measured serum sodium may be normal or slightly low despite
the marked hyperglycemia.
The corrected serum sodium is usually increased (add
1.6 meq to measured sodium for each 5.6-mmol/L [100-mg/dL]
rise inthe serum glucose). In contrast to DKA, acidosis and
ketonemia areabsent or mild.
A small anion-gap metabolic acidosis may be present
secondary to increased lactic acid.
Moderate ketonuria, if present, is secondary to starvation
29. HHNS: Diagnosis
History
Physical Examination
Lab test
BGL 600 to 1200mg/dL
Electrolytes
BUN
CBC- RBCs
Serum osmolality >350 mosm/kg
ABG analysis – PH normal
30. Management of DKA or HHS
The overall approach to the treatment of HHNS is similar
to that of DKA:
Fluid replacement,
Correction of electrolyte imbalances, and
Insulin administration
31. Management of DKA or HHS
1.Replace fluids:
2–3 L of 0.9% NS in 1–3 hr; the reduce to 250–500 mL/h; change to
5% glucose
when plasma glucose reaches 250 mg/dl in DKA and 300mg/dl in
HHS. HHS requires
more fluid.Assess hydration status, BP and urine out put ferquently
Patients may need up to 6-10 liters of IV fluid per day
Initially 0.9% NaCl – 0.5 to 1L per hour for 2 to 3hrs.
Use 0.45% NaCl for the patients with hypertension or
hypernatremia or those at risk for heart failure
32. 1.Replace fluids…
When the BGL reaches 300 mg/dL or less, the IV fluid may be changed
to D5W to prevent a precipitous decline in the BGL.
Monitoring fluid volume status
Vital Signs- orthostatic changes in BP and PR
Lung assessment
Intake and out put
The calculated free water deficit (which averages 9–10 L) should be
reversed over the next 1–2 days (infusion rates of 200–300 mL/h of
hypotonic solution).
In patients taking diuretics, the potassium deficit can
be quite large and may be accompanied by magnesium deficiency.
Hypophosphatemia may occur during therapy and can be improved
by using KPO4 and beginning nutrition.
33. 2. Administer short-acting insulin:
Regular Insulin 10units IV and 10 units IM, stat, then 0.1 units/kg
per hour by continuous IV infusion OR 5 units, I.V,boluses every
hour.
If serum glucose does not fall by 50 to 70 mg/dL from the initial
value in the 2-3 hours, the insulin infusion rate should be doubled
every hour until a steady decline in serum glucose is achieved
Acidosis is reversed with insulin to inhibit fat break down, there by
stopping acid build up
34. Cont…
3. Potassium- All patients with DKA have potassium depletion
irrespective of the serum K+ level.
- If the initial serum K+ is <3.3 mmol/L ,do not administer insulin
until the K+ is corrected.
- If the initial serum K + is >5.3 mmol/L, do not supplement K+ until
the level comes to < 5.3.
- If K+ determination is not possible doelay intiation of K+
replacement until there is a reasonable urine put(>50 ml/hr)
- The serum potassium should be maintained between 4.0 and 5.0
meq/l
Add 40–60 meq/l of IV fluid when serum K+< 3.7 meq/L
Add 20- 40meq/l of IV fluid when serum K+ < 3.8 -5.2 meq/l
35. Cont…
4.Precipitant identification and treatment -noncompliance,
infection, trauma, infarction.
Initiate appropriate workup for precipitating event (cultures,
CXR, ECG)
5. Follow up of response- Blood glucose every 1–2 h, Urine
ketones every 4hr,electrolytes (especially K+) every 6 h for first
24 h.
6. Continuation of treatment – the above treatment should
continue until the patient is stable, ketone free.
7. Transition- Insulin infusion may be decreased to 0.05–0.1
units/kg per hour or 2-3 units,IV, hourly.
Overlap in insulin infusion and SC insulin injection for about 3 -
5hr
8. SC long acting Insulin – start SC NPH as soon as the patient
eats. Monitor bloog glucose evry 4- 6 hour and give correctional
doses of regular insulin when needed.
36. Cont…
When the patient is completely out of ketoacidosis, regular insulin is
given 4 hourly subcutaneously according to the random blood sugar
(RBG) level as follows:
If RBG > 250mg/dl 12 Units
If RBG - 180-250mg/dl 8 Units
If RBG - 120-180mg/dl 4 Units
IV fluid solutions with higher concentrations of glucose such as D5NS
or (D50, 0.45NS) are administered when BGLs reach 250-300 mg/dL
to avoid too rapid a drop in the BGL
RBG < 120 mg/dl
37. Cont…
Insulin must be infused continuously until subcutaneous
administration of insulin resumes
BGLs are usually corrected before acidosis is corrected.
Thus, IV insulin may be continued for 12-24 hrs until the serum
HCO3- level improves to at least 15 to 18 mEq/L and until the
patient can eat
NURSING ALERT
Bicarbonate should be avoided, because of precipitation of sudden
hypokalemia
38. DKA: Nursing Management
Monitoring fluid and electrolyte status, BGLs, ECG, V/S, ABGs
and other clinical findings
Administering fluids, insulin
Prevent other complications such as fluid over load
As DKA resolved and potassium replacement rate is decreased, the
nurse makes sure that:
There are no signs of hyperkalemia on the electrocardiogram (tall,
peaked or tented T-waves)
The laboratory, values of potassium are normal or low
The patient is urinating (i.e. no renal shut down)
As the patient recovers, the nurse reassess the factors that may
have led to DKA and teach the patient and family
39. HHNS
Is a metabolic disorder of T2D resulting from a relative effective
insulin deficiency (i.e., Insulin resistance) initiated by an inter-
current illness that raises the demand for insulin, associated with
polyuria and sever dehydration.
Occurs most often in older people (50 to 70 years of age) who
have no known history of diabetes or who have type 2 diabetes
40. Cont…
Nursing Management of Patients with DM
Assessment
Care Plan
Nursing Diagnoses with interventions
1. Fluid Volume deficient may be related to, osmotic diuresis,
excessive gastric losses: diarrhea, vomiting, or restricted intake:
nausea, confusion, evidenced by weakness; thirst; sudden weight
loss, dry skin/mucous membranes, poor skin turgor, hypotension,
tachycardia, or delayed capillary refill
42. Nursing intervention: FVD
Administer fluids as indicate
Insert/maintain indwelling urinary catheter.
Monitor laboratory studies,
Administer potassium and other electrolytes via IV and/or by oral
route as indicated.
Insert NG tube and attach to suction as indicated
43. Cont…
Imbalanced Nutrition, less than body requirements may be
related to, insulin deficiency, decreased oral intake: anorexia,
nausea, gastric fullness, abdominal pain; altered consciousness,
hypermetabolic state: release of stress hormones (e.g.,
epinephrine, cortisol, and growth hormone), infectious process
evidenced by increased urinary output, dilute urine; reported
inadequate food intake, lack of interest in food; recent weight
loss; weakness, fatigue, poor muscle tone; diarrhea; increased
ketones.
44. Nursing interventions
Weigh daily or as indicated.
Ascertain patient’s dietary program and usual pattern; compare
with recent intake.
Auscultate bowel sounds. Note reports of abdominal
pain/bloating, nausea, vomiting of undigested food.
Provide liquids containing nutrients and electrolytes as soon as
patient can tolerate oral fluids; progress to more solid food as
tolerated.
Identify food preferences, including ethnic/cultural needs.
Include so in meal planning as indicated.
Observe for signs of hypoglycemia
45. Cont…
Monitor laboratory studies, e.g., serum glucose, acetone, pH,
HCO3.
Administer regular insulin by intermittent or continuous IV
method
Administer glucose solutions, e.g., dextrose and half-normal
saline.
Consult with dietitian for initiation of resumption of oral intake.
Provide diet of approximately 60% carbohydrates, 20% proteins,
20% fats in designated number of meals/snacks
46. Cont…
Risk for infection related to high glucose levels, decreased
leukocyte function, alterations in circulation; preexisting
respiratory infection, or UTI.
Nursing interventions
Observe for signs of infection and inflammation, e.g., Fever,
flushed appearance, wound drainage, purulent sputum, cloudy
urine.
Promote good hand washing by staff and patient.
Maintain aseptic technique for procedure
Provide catheter/perineal care. Teach the female patient to
clean from front to back after elimination.
47. Cont…
Provide conscientious skin care
Auscultate breath sounds.
Place in semi-fowler’s position.
Reposition and encourage coughing/deep breathing
Provide tissues and trash bag in a convenient location for sputum
and other secretions
Encourage/assist with oral hygiene.
Encourage adequate dietary and fluid intake
Administer antibiotics as appropriate
49. Diabetes mellitus: Complications
Diabetes-related complications usually do not appear until the
second decade of hyperglycemia.
Because type 2 diabetes mellitus (DM) often has a long
asymptomatic period of hyperglycemia before diagnosis, many
individuals with type 2 DM have complications at the time of
diagnosis.
Fortunately, many of the diabetes-related complications can be
prevented or delayed with early detection, aggressive glycemic
control, and efforts to minimize the risks of complications.
50. Cont…
Diabetes-related complications can be divided into
vascular and nonvascular complications and are similar
for type 1 and type 2 DM
Nonvascular complications include gastroparesis,
infections, skin changes, and hearing loss.
The vascular complications of DM are further subdivided
into microvascular (retinopathy, neuropathy, nephropathy)
macrovascular complications (coronary heart disease
[CHD], peripheral arterial disease [PAD], cerebrovascular
disease).
51. GLYCEMIC CONTROLAND COMPLICATIONS
The microvascular complications of both type 1 and type 2 DM
result from chronic hyperglycemia
Evidence implicating a causative role for chronic hyperglycemia
in the development of macrovascular complications is less
conclusive.
CHD events and mortality rate are two to four times greater in
patients with type 2 DM and correlate with fasting and
postprandial plasma glucose levels as well the
52. Cont…
The general categories of long-term diabetic complications:
A. Macrovascular disease
B. Microvascular disease, and
C. Neuropathy
The specific causes and pathogenesis of each type of complication
are still being investigated
53. Cont…
Macro Vascular Complications (Macroangopathy)
Can be seen both in diabetic and non-diabetic patients
Result from changes in the medium to large blood vessels
Blood vessels walls thicken sclerose and become occluded by
plaque that adheres to the vessel walls, and eventually blood flow
is blocked.
54. Cont…
Blood vessel walls thicken, scleroses
Occlusion by plaque that adheres to the vessel walls
Blood flow is blocked
Coronary artery disease Cerebrovascular disease
Peripheral vascular disease
Diminished peripheral pulses
Intermittent claudication (pain in the buttock, thigh, or calf during
walking
GANGRENE AMPUTATION
55. Micro Vascular Complications
Are unique to diabetes
Two areas affected:
A. Retina resulting in diabetic retinopathy
B. Kidneys resulting in diabetic nephropathy
Retinopathy Occurs because of changes in the microvasculature:
microaneurysms,
intraretinal hemorrhage,
Focal capillary closure
56. Cont…
Retinopathy has three main stages:
Nonproliferative (background),
Preproliferative, and
Proliferative widespread vascular changes (proliferation of new
blood vessels growing from the retina into the vitreous) and loss
of nerve fibers