Nursing care of patients with ENCEPHALOPATHY.pptx

Brain tissue damage

1. Encephalopathy

2. Introduction Encephalopathy means brain disease, disorder, or damage. The term refers to temporary or permanent conditions that affect the brain’s structure or function . Encephalopathy is a general term that refers to brain disease, damage, or malfunction. The major symptom of encephalopathy is an altered mental state. Encephalopathy is often considered a complication of a primary problem such as alcoholic cirrhosis, kidney failure, or anoxia.

3. Definition Encephalopathy is a term that refers to brain disease, damage, or malfunction. Encephalopathy can present a very broad spectrum of symptoms that range from mild, such as some memory loss  or subtle personality changes, to severe, such as dementia,  seizures,  coma, or death. In general, encephalopathy is manifested by an altered mental state that is sometimes accompanied by physical manifestations (for example, poor coordination of limb movements).

4. TYPES REVERSIBLE Hepatic Hashimoto Metabolic Wernicke's encephalopathy  Bovine spongiform encephalopathy Shigella  encephalopathy  IRREVERSIBLE Chronic Traumatic Hypoxic Ischemic

5. Hepatic encephalopathy -  When your liver is unable to remove toxins from your blood as well as it should, they build up in your body. That makes it hard for your brain to work well. It can happen to people with a chronic liver disease like cirrhosis or after an overdose of acetaminophen or other medications . Hashimoto’s encephalopathy.  This type is linked to a thyroid condition called Hashimoto’s disease. The cause isn’t clear, but it may be that your immune system attacks your brain and changes the way it works .

6. Metabolic encephalopathy.  This happens when another health condition, such as diabetes, liver disease, kidney failure, or heart failure, makes it hard for the brain to work. For example, if blood sugar gets too high in diabetes, it can lead to confusion and even a coma . Bovine spongiform encephalopathy (BSE) or "mad cow disease" (ataxia, dementia, and myoclonus or muscle twitching without any rhythm or pattern ) Shigella  encephalopathy (headache, stiff neck, delirium, seizures, coma ) Wernicke's encephalopathy (mental confusion, memory loss, decreased ability to move eyes)

7. Chronic traumatic encephalopathy-  This condition is caused by repeated head injuries, which damage the brain. Today, it’s best known for its ties to high-impact sports like football and boxing . Hypoxic-ischemic encephalopathy.  It happens when your brain doesn’t get enough oxygen, which leads to brain damage. It can happen after cardiac arrest, carbon monoxide poisoning, drug overdose, or near-drowning .

8. Introduction Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease. It is a life threatening complication of liver disease , occurs with profound liver failure and may result from the accumulation of ammonia and other toxic metabolites in the blood. As it progresses, confusion is followed by coma .

9. Epidemiology Approximately35 % of all patients with cirrhosis of the liver die in hepatic coma

10. Etiology Decrease in hepatocellular function Hypoxia Infection Diuretics (produce hypokalemia, alkalosis and hypovolemia ) Depressants :- phenobarbital, narcotics, tranquilizers and sedatives Gastrointestinal bleeding Medications containing ammonium or amino compounds Increased protein intake Constipation Dehydration  

11. PATHOPHYSIOLOGY

12. Clinical Manifestation Change of intellect, personality, emotion and consciousness with or without neurological sign. The degree of encephalopathy can be graded from 1 to 4. Grade :- 1 Poor concentration slurred speech, disordered sleep rhythm Grade :- 2 Drowsy but easily rousable , occasional aggressive behavior lethargic

13. Grade :-3 Marked confusion drowsy , sleepy but responds to pain and voice, gross disorientation Grade :-4 Unresponsive to voice , may or may not respond to painful stimuli, unconscious. Earliest feature are very mild and easily overlooked but as the condition becomes more severe , apathy, inability to concentrate, confusion, disorientation, drowsiness, slurring of speech and eventually coma develop. Convulsion sometimes occur.

14. Stage of Hepatic Encephalopathy S tage :- 1 Fatigue Restlessness Irritability Decreased intellectual performance Decreased attention span Diminished short term memory Personality change Sleep pattern reversal Stage :- 2 Deterioration in handwriting Asterixis (flapping tremor jerky movement of hand specially present in HE) Drowsiness Confusion Lethargy Pruritus Fetor hepaticus (musty odour due to presence of circulating methionine )

15. Stage :- 3 Severe confusion Inability to follow commands Deep somnolence, but rousable Stage :- 4 Coma Unresponsive to painful stimuli Possible decorticate or decerebrate posturing

16. Diagnostic Evaluation History collection Physical examination:- flapping tremor inability to perform simple mental arithmetic task or draw object such as star Arterial amonia is usually increased As condition progress hyper- reflexia , bilateral extensor plantar responses. Sweet and fruity smell from breath EEG :-show generalized slowing , an increase in amplitude of brain waves and characteristic

17. Management The principles of management for HE are to treat or remove the causative factor and to suppress the production of neurotoxins by bacteria in the bowel . Medical management Lactulose (15-30 ml 8 hourly) is a disaccharide which is taken orally and reaches the colon intact, to be metabolised by colonic bacteria. The dose is increase slowly until bowel is moving twice daily. It produces an osmotic laxative effect , reduces pH of the colonic content, thereby limiting colonic ammonia absorption and promotes the incorporation of nitrogen into bacteria.

18. Neomycin (1-4 g 4-6 hourly) is an antibiotic which acts by reducing the bacterial content of the bowel. It can be used in addition or as alternative to lactulose intolerance Dietary protein restriction is rarely needed and is no longer recommended as first line treatment because it is unpalatable and can lead to worsening nutritional state in already malnourish patient.

19. Surgical management Liver transplantation surgery is indicated for chronic or refractory hepatic encephalopathy

20. Nursing Management History taking Physical Examination Assess for changes of intellect, personality, emotions and consciousness Assess for severe apathy, inability to concentrate, confusion and disorientation drowsiness, slurring of speech and coma Bilateral extensor planter response Paraplegia dementia Assess the result of ABG, electrolyte level

21. Nursing Diagnosis Deficient fluid volume related to bleeding, decreased intake and ascites as evidence by physical examination Ineffective breathing pattern related to hypoxia Imbalanced nutrition less than body requirement related to GI adverse effect Risk for injury related to loss of protective mechanism secondary to hepatic coma

22. Activity intolerance Self-care deficit Disturbed sleep pattern Impaired verbal communication Risk for aspiration Impaired gas exchange Impaired tissue integrity Disturbed sensory perception Other Nursing Diagnosis

23. Interventions Fluid balance must be balanced hence should start Intravenous therapy Maintained and monitor to prevent further hepatic injury and reduced renal perfusion Monitor vital sign frequently Measure urine output hourly Monitor electrolyte and acid base balance because its disturbances such as hypokalemia and alkalosis may precipitate hepatic encephalopathy

24. Hepatic coma may create a multitude of problem for the client with encephalopathy. Prevent hypoxemia (to prevent and treat hypoxemia, attend to respiratory intervention like maintain airway. Prevent nosocomial infection Prevent ammonia toxicity and hypokalemia Prevention to the injuries

25. WERNICKE’S ENCEPHALOPATHY

26. Introduction Acute neurological disorder induced by Thiamine deficiency(Vitamin B1) More prevalent in males (1.7: 1) Average onset age is 50 years (range: 30-70 years) First described in 1881 by Dr. Carl Wernicke Rate has been found to be significantly higher in specific populations, i.e., homeless people, older people (especially those living alone or in isolation), and psychiatric inpatients, where alcohol use and poor nutritional states predominate. Prevalence at autopsy exceeds clinical detection .

27. Thiamine (Vitamin B1) Water soluble vitamin absorbed from the gut. Serves as a cofactor to several enzymes that are responsible for lipid and carbohydrate metabolism, production of amino acids and production of glucose derived neurotransmitters. Also have a role in axonal conduction esp. of acetylcholinergic and serotoninergic neurons . Cellular impairment and injury occur within 2- 3 weeks of decreased intake and thiamine depletion. Acute thiamine deficiency leads to mitochondrial dysfunction resulting in oxidative toxicity in areas of brain.

28. Etiology Chronic alcoholism Malnutrition or prolonged starvation Hyperemesis Gravidarum Bariatric surgery Gastric malignancy (inflammatory bowel disease) Intestinal obstruction (abscess) Thyrotoxicosis

29. Iatrogenic (IV glucose without thiamine supplement or chronic hemodialysis) Systemic diseases (AIDS, disseminated TB) Thiamine deficient formula/ breastfeeding by mothers with inadequate thiamine intake Infection ( precipitating factor)- pneumonia, meningitis

30. Clinical Triad – Ocular Abnormalities ( 29%) Encephalopathy (82%) Ataxia (23%)

31. Ocular Abnormalities Nystagmus , bilateral rectal palsies and conjugate gaze palsies (involvement of oculomotor , abducens and vestibular nuclei) Less common manifestations are pupillary abnormalities, ptosis .

32. Encephalopathy (82%) Global confusion state, disinterest, inattentiveness or agitation. Most common presentation is mental state changes. Stupor and coma observed in severe cases

33. Ataxia Due to polyneuropathy, cerebellar damage and vestibular paresis. Wide based stance Slow and uncertain short stepped gait. Inability to walk without support in severe cases .

34. Other symptoms Peripheral neuropathy (weakness, foot drop & decreased proprioception) GI symptoms (nausea, vomiting, lactic acidosis) Hypotension Hypothermia Memory disturbances

35. Diagnostic evaluations Detailed patient history Physical and neurological examination Laboratory evaluation CBC (rule out infections, severe anemia) Serum thiamine levels Serum glucose levels Toxic drug screening Lumbar puncture (rule out CNS infections )

36. Imaging MRI (fluid attenuated inversion recovery {FLAIR} images) CT ( not specific) EEG ( rule out non- convulsive status epilepticus )

37. Management Considered a medical emergency Emergency care : Parenteral Thiamine (multiple daily doses – 500mg/dose) Alcohol withdrawal In case of WKS, use of oral Thiamine to prevent further complications. Parenteral magnesium sulfate in case of hypomagnesaemia Balanced diet with high thiamine containing foods.

38. UREMIC ENCEPHALOPATHY

39. Uremic encephalopathy Resembles any other metabolic and toxic disorders of CNS. Etiology- Consequences of uremia Dialysis Thiamine deficiency Drug toxicity Transplant rejection. Encephalopathy and renal impairment may both relate independently to the same underlying systemic illness Diabetes Connective tissue diseases .

40. Uremic encephalopathy most commonly relates to : a variety of metabolic abnormalities with the accumulation of numerous metabolites imbalance in excitatory and inhibitory neurotransmitters, and hormonal disturbances leading to cerebral dysfunction.

41. Metabolite abnormalities: 90 compounds considered to be uremic toxins. Retention of urea occurs. Accumulation of guanidine compounds ( guanidinosuccinic acid, methylguanidine , guanidine, and creatinine ) cause uremic seizures and cognitive dysfunction. Guanidinosuccinic acid accumulation (may inhibit transketolase , a thiamine-dependent enzyme) affects the maintenance of myelin. Low-level aluminum overload in renal failure causes gradual deterioration in cerebral function .

42. Neurotransmitter and Receptor abnormality : Activation of N-methyl-d-aspartate (NMDA) receptors and inhibition of γ- aminobutyric acid-A (GABA-A) transmission may be involved. Abnormalities of the membrane pumps, both Na+, K +, ATPase and calcium ions

43. Hormonal changes in uremic encephalopathy elevated serum concentrations of parathyroid hormone growth hormone Prolactin luteinizing hormone , insulin glucagon

44. Clinical Manifestations The clinical features of the encephalopathy include : Waxing and waning impairment of external awareness. Ability to concentrate is impaired: P atients seem preoccupied Apathetic P oor attention span B ecome increasingly disoriented E xhibit emotional lability S leep inversion.

45. With progression, patients become more obtunded Delusions , illusions, and hallucinations (typically visual) develop. Patients may develop an acute delirium Appear to be agitated and excited. – Eventually replaced by stupor and coma.

46. Seizures are common. They are usually Generalized convulsions In acute renal failure, seizures occur within days of onset ( oligoanuria ). In chronic renal failure, they occur with advanced disease, often preterminally May be multiple,

47. Lab Investigations include- RFT CSF EEG Brain Imaging . Laboratory studies provide evidence of impaired renal function but are of limited utility in monitoring the course of the encephalopathy. Furthermore , abnormal renal function tests do not exclude other causes of encephalopathy. An underlying structural lesion must be excluded in uremic patients especially after seizures.

48. Impact of Immediate Nursing Care for Hepatic Encephalopathy Patients to Reduce Gastrointestinal Complication on Patient's Outcome in Intensive Care Unit Immediate care is an essential nursing function to identify early deterioration in mental status. The nurse monitors the patient's mental status closely . Oxygen is administered if oxygen de-saturation occurs. The nurse monitors for fever or abdominal pain. This may be a signal the onset of bacterial peritonitis or other infection. Aim- The aim of the study was to investigate the immediate nursing care for hepatic encephalopathy patients' to reduce gastrointestinal complication on patient's outcome. Subject and methods descriptive research design was used to conduct this research . The sample of this study was consisted of 60 patients. Tools used in this study comprised three main tools .

49. Tool 1:- Patients assessment sheet. Tool 11 :- Fluid intake and| output and nutrition assessment. Tool 111:- Evaluation sheet . R esult :- Regarding West- haven criteria there was a significant decrease for the studied group from1st day and 2nd day. There were statistical significance differences between the two days. Regarding complete blood picture ; WBC in the studied group showed that significant decrease on 2nd day. Fluid intake & output in the studied group showed that significant increase on 2nd day.

50. Conclusion : Applied immediate nursing care significant to reduce gastrointestinal complication in hepatic encephalopathy patients and improve the patient's outcome . Therefore , it is recommended to providing nutritional counseling for all patients with hepatic encephalopathy , continuing Educational Nursing Programmes to access the high quality of care.

51. https:// www.medicalnewstoday.com/articles/324008#symptoms-of-encephalopathy https://www.webmd.com/brain/what-is-encephalopathy#:~:text=There%20are%20two%20main%20types%20of%20encephalopathy%3A%20reversible%20and%20irreversible .