Hepatic Encephalopathy And Dka
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Diabetic Ketoacidosis -
is caused by an absent or markedly inadequate amount of insulin
-
results in disorder in the metabolism of carbohydrate, protein and fat
3 main clinical features of DKA: •
*hyperglycemia
•
*dehydration and electrolyte loss
•
*acidosis
Assessment and Diagnostic findings: •
*blood glucose
•
*serum bicarbonate
-300 to 800 mg/dl -0-15mEq/L
•
*serum pH -low: 6.8-7.3
•
*PCO2 -low: 10-30mmHg
• •
compensation for acidosis and in the urine *electrolyte depletion *BUN, creatinine, hgb and hct
- increased breakdown of fat •
- increased fatty acids
-reflects respiratory *ketone bodies -elevated in the blood -elevated due to water loss - lack of insulin -decreased utilization of glucose by muscle, fat and liver
•
- increased ketone bodies
•
- acidosis dehydration
-increased production of glucose by liver -acetone breath -poor appetite hyperglycemia -nausea, blurred vision, polyuria -nausea -weakness -vomiting -headache -abdominal pain increased thirst - increasingly rapid
respirations
Prevention: •
a. full compliance to the medical treatment of diabetes mellitus
•
b. good hydration
•
c. good nutrition
•
d. monitoring of blood and urine ketones every 3-4 hours
Management: •
a. rehydration >6-10 L of IVF >plain NSS or half
strength saline • b. restoring electrolytes monitoring
>ECG *reversing acidosis: -insulin
Nursing management: •
*normalize insulin activity and blodd glucose levelsto reduce the development ofvascular and neurophatic complications.
•
* conventional treatment (one or two injection per day)
• •
* intensive treatment ( three or four insulin injection per day or insulin pump therapy plus frequent blood glucose monitoring and weekly contact with diabetes educators.) nutrional management (control total caloric intake)
•
* exercise
•
health teaching
HEPATIC ENCEPHALOPATHY Is due to increased AMMONIA levels. The liver cannot convert ammonia by products of protein metabolism into Urea Hepatic coma •
-The initial manifestations are BEHAVIORAL changes and MENTAL changes.
Advance Stage : Asterixis (flapping tremor of hand) •
Confusion / disorientation
•
Delirium / hallucination
Pathophysiology: Ammonia accumulates because damaged liver fail to detoxifyand convert to urea the ammonia that is constantly entering the bloodstream. Ammonia enters the bloodstream as it result of absorption from the GI tract and its liberation from kidney and muscle cells. The increased ammonia concentration in the blood causes brain dysfunction and damage, resulting in hepatic encephalopathy.
Signs and Symptoms:
•
• minor mental changes • motor disturbances • slightly confused • alteration in mood • restlessness • insomia at night flaccid replexes
Assessment and Diagnostic Findings: •
EEG ( show generalized slowing, an increase in the amplitude of brain waves and characteristic triphasic waves.)
•
Fetor hepaticus ( sweet, slightly fecal odor to the breath.)
Medical Management: •
Lactulose ( to reduce serum ammonia levels)
•
Vitamins supplementation ( vit. A, D, E, K)
•
Benzodiazepines antagonist
•
Neomycine sulfate
Summary of Collaborative Management: •
Rest. To reduce metabolic demands of the liver.
•
Diet • •
•
Early stage − High calorie, HIGH carbohydrates, LOW protein that is restricted to complete protein only, moderate fats. Late stage
HIGH calorie, HIGH carbohydrates, LOW protein. •
Skin care
•
Avoid trauma/injury
•
Prevent infection
•
Decrease Ammonia formation − Restrict protein in the diet − Duphalac (lactulose) − Neomycin sulfate − Colchicine − Tap water or NSS enema
•
Avoid sedatives and paracetamol.
•
Avoid ASA.
•
Avoid Hypokalemia
Manage Ascites Monitor weight, intake and output, abdominal girth Restrict sodium and fluid intake Administer diuretics as ordered Initially, K – sparring diuretic Later, K- wasting diuretic •
Administer albumin / IV as ordered assist in paracentesis
•
Abdominal Paracentesis • Withdrawal of fluid from the peritonealspace • Purpose: diagnostic and therapeutic • Pretest: consent, empty bladder • Position: sitting • Site: midway between the umbilicus and symphysis
•
Intratest: 1,500 ml maximum amount collected at one time, Monitor VS
•
Post-test: monitor VS, bleeding complication − Measure abdominal girth and weight
is caused by an absent or markedly inadequate amount of insulin
-
results in disorder in the metabolism of carbohydrate, protein and fat
3 main clinical features of DKA: •
*hyperglycemia
•
*dehydration and electrolyte loss
•
*acidosis
Assessment and Diagnostic findings: •
*blood glucose
•
*serum bicarbonate
-300 to 800 mg/dl -0-15mEq/L
•
*serum pH -low: 6.8-7.3
•
*PCO2 -low: 10-30mmHg
• •
compensation for acidosis and in the urine *electrolyte depletion *BUN, creatinine, hgb and hct
- increased breakdown of fat •
- increased fatty acids
-reflects respiratory *ketone bodies -elevated in the blood -elevated due to water loss - lack of insulin -decreased utilization of glucose by muscle, fat and liver
•
- increased ketone bodies
•
- acidosis dehydration
-increased production of glucose by liver -acetone breath -poor appetite hyperglycemia -nausea, blurred vision, polyuria -nausea -weakness -vomiting -headache -abdominal pain increased thirst - increasingly rapid
respirations
Prevention: •
a. full compliance to the medical treatment of diabetes mellitus
•
b. good hydration
•
c. good nutrition
•
d. monitoring of blood and urine ketones every 3-4 hours
Management: •
a. rehydration >6-10 L of IVF >plain NSS or half
strength saline • b. restoring electrolytes monitoring
>ECG *reversing acidosis: -insulin
Nursing management: •
*normalize insulin activity and blodd glucose levelsto reduce the development ofvascular and neurophatic complications.
•
* conventional treatment (one or two injection per day)
• •
* intensive treatment ( three or four insulin injection per day or insulin pump therapy plus frequent blood glucose monitoring and weekly contact with diabetes educators.) nutrional management (control total caloric intake)
•
* exercise
•
health teaching
HEPATIC ENCEPHALOPATHY Is due to increased AMMONIA levels. The liver cannot convert ammonia by products of protein metabolism into Urea Hepatic coma •
-The initial manifestations are BEHAVIORAL changes and MENTAL changes.
Advance Stage : Asterixis (flapping tremor of hand) •
Confusion / disorientation
•
Delirium / hallucination
Pathophysiology: Ammonia accumulates because damaged liver fail to detoxifyand convert to urea the ammonia that is constantly entering the bloodstream. Ammonia enters the bloodstream as it result of absorption from the GI tract and its liberation from kidney and muscle cells. The increased ammonia concentration in the blood causes brain dysfunction and damage, resulting in hepatic encephalopathy.
Signs and Symptoms:
•
• minor mental changes • motor disturbances • slightly confused • alteration in mood • restlessness • insomia at night flaccid replexes
Assessment and Diagnostic Findings: •
EEG ( show generalized slowing, an increase in the amplitude of brain waves and characteristic triphasic waves.)
•
Fetor hepaticus ( sweet, slightly fecal odor to the breath.)
Medical Management: •
Lactulose ( to reduce serum ammonia levels)
•
Vitamins supplementation ( vit. A, D, E, K)
•
Benzodiazepines antagonist
•
Neomycine sulfate
Summary of Collaborative Management: •
Rest. To reduce metabolic demands of the liver.
•
Diet • •
•
Early stage − High calorie, HIGH carbohydrates, LOW protein that is restricted to complete protein only, moderate fats. Late stage
HIGH calorie, HIGH carbohydrates, LOW protein. •
Skin care
•
Avoid trauma/injury
•
Prevent infection
•
Decrease Ammonia formation − Restrict protein in the diet − Duphalac (lactulose) − Neomycin sulfate − Colchicine − Tap water or NSS enema
•
Avoid sedatives and paracetamol.
•
Avoid ASA.
•
Avoid Hypokalemia
Manage Ascites Monitor weight, intake and output, abdominal girth Restrict sodium and fluid intake Administer diuretics as ordered Initially, K – sparring diuretic Later, K- wasting diuretic •
Administer albumin / IV as ordered assist in paracentesis
•
Abdominal Paracentesis • Withdrawal of fluid from the peritonealspace • Purpose: diagnostic and therapeutic • Pretest: consent, empty bladder • Position: sitting • Site: midway between the umbilicus and symphysis
•
Intratest: 1,500 ml maximum amount collected at one time, Monitor VS
•
Post-test: monitor VS, bleeding complication − Measure abdominal girth and weight
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