Diabetic Ketoacidosis

Ivan T. Pacatang RN MN

Diabetic Ketoacidosis

an acute complication of DM type 1 characterized by: 1. Hyperglycemia 2. Ketonuria 3. Acidosis 4. Dehydration

Diabetic Ketoacidosis: Pathophysiology

1. Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat for fuel. 2. Free fatty acids, released from the metabolism of fat, are converted to ketone bodies in the liver 3. Ketone bodies are organic acids that cause metabolic acidosis

Diabetic Ketoacidosis: Pathophysiology

4. Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium, sodium, phosphate, and water

Diabetic Ketoacidosis

Clinical Manifstations:

Early Stage
Polydipsia, polyuria Fatigue, malaise, drowsiness Anorexia, N/V Abdominal pains, muscle cramps

Late Stage
Kussmaul respirations Fruity, sweet breath Hypotension, weak pulse Stupor and coma

Diabetic Ketoacidosis

DIAGNOSTIC EVALUATION:
1. Serum glucose elevated over 300 mg/dL up to 1,000 mg/dL 2. Serum and urine ketone bodies (+) 3. Serum HCO3 and pH = decreased pCO2 = decreased

4. Serum Na and K= low, normal or high 5. BUN, creatinine, hemoglobin, and hematocrit = elevated 6. Urine glucose (+) in high concentration Specific gravity is increased

Diabetic Ketoacidosis

MANAGEMENT:

I.V. fluids for fluid replacement I.V. insulin drip (regular insulin) Electrolyte replacement

Diabetic Ketoacidosis: NURSING INTERVENTIONS

Assess for signs of dehydration Monitor intake and Output Monitor urine specific gravity and blood glucose frequently Assess for symptoms of hypokalemia. Administer replacement electrolytes and insulin as ordered

Diabetic Ketoacidosis: NURSING INTERVENTIONS

Monitor serum glucose, bicarbonate, and pH levels Provide reassurance about improvement of condition and that correction of fluid imbalance will help reduce discomfort

Hyperglycemic Hyperosmolar Nonketotic Syndrome

Hyperosmolar Hyperglycemic Nonketotic Syndrome: Definition

an acute complication of DM type 2 characterized by hyperglycemia, dehydration, and hyperosmolarity, but with little or no ketosis

Hyperosmolar Hyperglycemic Nonketotic Syndrome: Pathophysiology

1. Prolonged hyperglycemia with glucosuria produces osmotic diuresis 2. Loss of H2O, Na and K results in severe dehydration, causing hypovolemia and hemoconcentration. 3. Hyperosmolarity d/t increased glucose and sodium 4. Insulin continues to be produced at a level that prevents ketosis

Hyperosmolar Hyperglycemic Nonketotic Syndrome: Pathophysiology

Increased blood viscosity causes tissue hypoxia.

Caused by inadequate amounts of endogenous/exogenous insulin to control hyperglycemia. Use of therapeutic agents that increase blood glucose levels (eg, glucocorticoids, immunosuppressive agents). Use of therapeutic procedures that cause stress or increase blood glucose levels (eg, hyperosmolar hyperalimentation, peritoneal dialysis).

Hyperosmolar Hyperglycemic Nonketotic Syndrome: Manifestations

Early Polyuria, dehydration Fatigue, malaise Nausea, vomiting

Late Hypothermia Seizures, stupor, coma Muscle weakness

Hyperosmolar Hyperglycemic Nonketotic Syndrome: Diagnostics

Diagnostics Evaluation Serum glucose and osmolality = elevated Serum and urine ketone bodies = minimal to absent Serum Na and K levels = may be elevated BUN and creatinine = may be elevated Urine specific gravity = elevated

Hyperosmolar Hyperglycemic Nonketotic Syndrome: Management 1. Correct fluid and electrolyte imbalances with I.V. fluids

2. Provide insulin via I.V. drip to lower plasma glucose 3. Evaluate complications, such as stupor, seizures, or shock, and treat appropriately 4. Identify and treat underlying illnesses or events that precipitated HHNS

Hyperosmolar Hyperglycemic Nonketotic Syndrome: Complications 1. Too rapid infusion of I.V. fluids can cause cerebral edema and death 2. HHNS is a medical emergency that, if not treated properly, can cause death 3. Patients who become comatose will need nasogastric (NG) tubes to prevent aspiration

Criteria

DKA

HHS

Age S/Sx
PA

Dxtics Onset Mortality

Any age 3Ps, orthopneic hypotension, LOC changes, N/V Dry flushed skin, poor turgor, decreased BP, dry mucous membranes, Kussmauls respiration and acetone breath Glucose, Ketones(+), BUN, Creatinine, WBC Hours to days
<10

> 50 yrs old Same as DKA but has a slower onset Same with DKA but without Kussmauls respiration and acetone breath Ketones absent, WBC normal with infection Days to weeks
10 25%

Pheochromocytoma

pheochromocytoma

A benign tumor
Originates from the chromafn cells of the adrenal medulla 80% to 90%, tumor arises in the medulla 10% occurs in the extra-adrenal chromafn tissue near the aorta, ovaries, spleen, or other organs

pheochromocytoma

May occur at any age (peak: 40 and 50 years) Affects men and women equally High incidence in family members 10% are malignant

Pheochromocytoma: Signs and Symptoms

Typical triad of symptoms: headache, diaphoresis and palpitations HPN and cardiovascular disturbances Tremor, headache, ushing, and anxiety Hyperglycemia results from glycogenolysis (may need insulin to control glucose levels)

Pheochromocytoma: Signs and Symptoms

acute, unpredictable attacks: seconds to hours duration Manifestations: extremely anxious, weak, headache, vertigo, blurring of vision, tinnitus, air hunger, and dyspnea, polyuria, nausea, vomiting, diarrhea, abdominal pain, and a feeling of impending doom.
Palpitations and tachycardia BP exceeds 250/150 mmHg

pheochromocytoma

5 Hs of Assessment:
Hypertension Headache Hyperhidrosis (excessive sweating) Hypermetabolism Hyperglycemia

Pheochromocytoma: Laboratory Examinations

Urinary catecholamine metabolites measurements (metanephrines [MN] and vanillylmandelic acid [VMA]) or free catecholamines are the standard diagnostic tests 24-hour urine specimen Medications and foods (eg, coffee, tea, bananas, chocolate, vanilla, aspirin) may alter the results of these tests Anti HPN drugs are not given prior to testing of urine

pheochromocytoma

CT scans, MRI, and ultrasound to localize disease and to assess number of tumors 131I-metaiodobenzylguanidine (MIBG) scintigraphy: determines location of tumor and metastasis MIBG: a specic isotope for catecholamine-producing tissue MIBG scintigraphy is: noninvasive, safe has increased the accuracy of diagnosing tumors

Management

Patient is placed on bed rest with the head of the bed elevated to promote an orthostatic decrease in blood pressure ICU for monitoring of ECG administration of alpha - adrenergic blocking agents or smooth muscle relaxants to lower BP

Management

Phenoxybenzamine (Dibenzyline), long-acting alpha-blocker if BP is stable for surgery Beta-adrenergic blocking agents used in patients with dysrhythmias

Management

Hypotension and hypoglycemia may occur postOP Manipulation of glands during surgery (?) Corticosteroid therapy (?)

Chronic Renal Failure

CRF

A large proportion of the nephrons are damaged due to acute or chronic kidney disease Nephrons die off, the undamaged ones increase their work capacity Pt may have signicant kidney damage without showing symptoms of renal failure

CRF: CAUSES

Hypertension (prolonged & severe) Diabetes mellitus Glomerulopathies (from SLE and other disorders) Nephritis Hereditary renal disease Obstructive uropathy Developmental or congenital disorder

CRF: Consequences of Decreasing Renal Function

1. Progression varies on underlying cause & severity 2. Stages: decreased renal reserve, renal insufficiency, renal failure, ESRD 3. Retention of Na and H2O 4. Decreased GFR (RAAM)

CRF: Consequences of Decreasing Renal Function

5. Metabolic acidosis 6. Decreased GFR increases phosphate, with reciprocal decrease in serum Ca & bone resorption of Ca 7. Erythropoietin decreases 8. Uremia affects CNS

CRF: Clinical Manifestations

GI: anorexia,N/V, hiccups, ulcers and hemorrhage Cardiovascular: hyperkalemia, HPN, pericarditis, pericardial effusion and tamponade Respiratory: pulmonary edema, pleural effusions and rub Neuromuscular: fatigue, sleep disorders, headache, lethargy, muscular irritability, peripheral neuropathy, seizures, coma Metabolic and endocrine: glucose intolerance, hyperlipidemia, sex hormone disturbances

CRF: Clinical Manifestations FE & acid base: salt and water retention, acidosis, hyperK, hypocalcemia Hematologic: anemia, defect in quality of platelets, increased bleeding tendencies Psychosocial: personality and behavior changes, alteration in cognitive processes

CRF: Diagnostic Evaluation Complete blood count : anemia Elevated creatinine, BUN, phosphorus Decreased Ca, HCO3 and CHONs (albumin) ABG level: low blood pH, low pCO2 &HCO3 24-hour urine for creatinine, protein, creatinine clearance

CRF: Nursing Diagnoses Excess Fluid Volume Imbalanced Nutrition: Less Than Body Requirements Impaired Skin Integrity Constipation Risk for Injury Ineffective Therapeutic Regimen Management

CRF: Nursing Interventions GOAL: Conservation of renal function Maintain F/E and acid base Maintain Nutrition Maintain Skin Integrity Detection of reversible cause and Rx Treatment of Anemia Dialysis Renal Transplant

CRF

DIET
Calories :high Protein: restricted but increased in dialysis Sodium: restricted to minimize Na and uid retention Potassium: restricted @ late stage Calcium: increased d/t poor absorption r/t faulty vitamin D activation Phosphorus: restricted d/t high blood levels r/to hypocalcemia Saturated fat and cholesterol: restricted Fluids: restricted

CRF

-fin-