CLINICAL CLCD CASE STUDY & nursing care PLAN

CLCD CACE STUDY FOR NURSING STUDENT

1. Name: J.C.D.FERIX Date: Institution: SHSHC A Clinical Case Study

2. Case Study Overview PT NAME:-S.SIVAKUMAR AGE:-49 SEX:-M RELIGION:-HINDU MARITAL STATUS:-M OCCUPATION:-ELECTRIC BORD PRESENT ADDRESS:-KILINOCHCHI AD.HOSPITAL:-EVERGREEN HEALTH CLINIC MEDICAL WARD DOA:-15/10/[email protected] DOD:-25/10/[email protected]

3. Generalized abdominal swellingwith discomfort ,heaviness. for 2 months. chest pain joint pain,skin rash, pigmentation difical urine for scrotal&penile edema Scanty micturition with constipation for 1 month. generalized weakness for 1 month fever 2 days R/upper thigh abscess B/L LL swelling Then he had admitted in this hospital for proper management.,,,.................P.T.O...... P/C

4. PT/co-morbidities HTN (clinic DGH KIL) NON DM/ HF/RF/ PT Hx:- smoker,alcoholic,betel leaf & betel nut chewing for about 20 years. Allergy Hx:- He wasn’t allergic to any specific food or aero allergen or drugs. PSHx:- nill family Hx:- His father& mother has been died due to geriatric illness.He had no family history of liver disease,hypertension,diabetes or any other familial diseases.His family member was five including his wife.All of them are alive & healthy.

5. Appearance :Ill looking; pinched face,sunken eyes, hollowed temporal fossa,shallow & dry face. Body Built : Emaciated. Nutrition : Undernourished Decubitus : On choice Anaemia : Mil Jaundice : Mild Cyanosis : Absent Clubbing : Absent Koilonychias: Absent Leuconychia: Present Oedema : Bipedal pitting oedema presen Dehydration : Mild Pigmentation: mild Palmer Erythema : mild GENERAL EXAMINATION FOR HEAD TO TOE ASSEMENT

6. Dupuytren’s Contracture : Absent  Flapping Tremor : present Gynecomastia : present Lymph Node : Not Palpable Thyroid Gland : Not Enlarged Body Hair Distribution :NOT Loss of body hair Pulse : 78 beats/min Blood Pressure : 120/70 mmhg Temperature : 98 °F Respiratory Rate : 16 breaths/min Weight : 57 kg Examination Of Gastrointestinal System:  a) Examination of mouth & oropharynx :- Lips,teeth,gum, buccal mucosa & palate look normal.Tongue looks pale

7. b) Abdomen Proper:- Inspection: ⭕ Size & shape: Distended, flanks are full. ⭕ Umbilicus : Transverse slit ⭕Visible vein : Absent ⭕Visible peristalsis: Absent ⭕ Scar mark & striae : Absent ⭕ Groin : Loss of pubic hair with negative cough impulse. Palpation:  Superficial : ⭕Temperature: heat for RUQ ⭕Tenderness : present ⭕Localized swelling: Absent ⭕Rigidity : Absent ⭕Muscle Guarding: Absent ⭕Abdominal Girth : Increased Deep :- ⭕Liver& Spleen : palpable. ⭕Kidneys : not ballot able ⭕Para aortic lymph node : couldn’t examine due to ascites.

8. ⭕Testes : both were swelling & tender ⭕Hernial orifices : intact Percussion :- ⭕ Shifting Dullness : Present ⭕Fluid thrill : Present Auscultation :- ⭕Bowel Sound : Presen Examination Of NervousSystem:  A)Higher Psychic Function: 1.Appearance & Behaviour : Ill looking, anxious 2.State of Consciousness : poor 3.Orientation with time,place & person: Oriented 4.Memory : A slight tendency of forgetfulness 5.Emotional state : Good 6.Speech & language : Normal  B)Examination Of All Cranial Nerves: 1.Olfactory Nerve : Intact 2.Optic Nerve : Intact 3.Oculomotor Nerve : Intact

9. 4 .Trochlear Nerve : Intact 5.Trigeminal Nerve : Intact 6.Abducent Nerve : Intact 7.Facial Nerve : Intact 8.Vestibulo-cochlear Nerve : Intact 9.Glossopharyngeal nerve : Intact 10.Vagus Nerve : Intact 11.Accessory Nerve : Intact 12. Hypoglossal Nerve : Intact C)Motor Functions: 1.Bullkof the muscle: Normal 2.Tone of the muscle: Normal 3.Power of the muscle: Normal 4.Involuntary movement (Tremor) : present 5.Coordination test : Coordinated 6.Gait & Posture : Normal 7.Reflexes (Superficial & Deep) : Intact  D)Sensory Functions: 1.Sense of touch : Intact

10. 2.Pain sensation : Intact 3.Temperature : Intact 4.Position Sense : Intact  E)Signs Of Meningeal Irritation: 1.Neck Rigidity : Absent 2.Kernig’s Sign : Absent 3.Brudzininski’s Sign : Absent Examination OfCardiovascular System: Pulse : 78 b/min;regular;catacrotic;condition of vessel wall is normal. Neck Veins : JVP not Raised  Blood Pressure : 120/70 mmhg  Precordium:  Inspection: ⭕ Any Chest Deformity : Absent ⭕Visible Cardiac Impulse : Absent ⭕Any Scar Mark : Absent  Palpation: ⭕Apex Beat : Left 5th intercostal space,9 cm away from midline

11. ⭕Thrill : Absent ⭕ Left Parasternal heave ; Absent ⭕ Palpable P2 : Absent  Auscultation: 1st & 2nd heart sounds are audible in all auscultatory area.There is no murmur or any other added sound Examination OfRespiratory System:  Inspection: ⭕ Shape of the chest: elliptical, bilaterally symmetrical. ⭕ Movement of the chest : Regular ⭕ Respiratory Rate : 16 b/min ⭕Visible impulse,scar mark,engorged vein: absent  Palpation: ⭕ Trachea: Central in position ⭕ Chest expansibility: Normal ⭕ Vocal fremitus : normal ⭕ Rib tenderness : Absent 

12. Percussion: ⭕Percussion note : Resonant  Auscultation: ⭕ Breath sound: Vesicular ⭕Vocal resonance : Normal ⭕ Added sound : Absent

13. Ix

14. date 15/10 17/10 19/10 21/10 24/10 26/10 WBC 10.11 10.5 8.64 7.59 6.87 9.54 HB 7.8 7.4 7.8 7.4 5.3 6.8 HCT 23.6 RBC 2.85 PLT 42 59 109 120 120 109 ESR 50 37 51 45 41.2 27 CRP 3.52 6.78 4.12 3.5 4.9 7.3 Scr 1.84 0.94 0.83 1.87 1.54 0.95 UREA 72.6 20.2 Na 132.5 133.2 140.4 132.1 133.4 133.8 K 6.33 3.9 3.2 2.4 5.5 5.2 CL 104.3 107.1 100.8 109.3 99.2 97.4 Ca 2.34 2.61 2.51 2.18 2.18 2.34 AST 106.4 134.7 129.6 75.7 68.9 100.87

15. ALT 217.8 115.6 100.6 101.6 97.9 48.0 GGT 98 109 75.4 98 103 55.3 TOT.BILL 8.7 5.6 6.3 4.9 5.4 5.0 DRIC.BILL 2.14 2.3 1.54 1.31 0.29 0.89 Sr.PROTEIN 4.77 3.23 4.97 3.21 4.34 5.12 ALBUMIN 2.07 1.64 1.53 0.98 2.65 3.01 GLOBULIN 4.26 3.1 CHOLEST 85.6 TRGLYCE 106.9 HDL 17.8 LDL 46.4 VLDL 21.4 PT 28.24 26.32 20.32 22.10 21.01 20.12 INR 1.77 2.67 1.37 2.81 1.36 1.37

16. OTHER Ix HBsAG:-neg HCV Ab:-neg VDRL:- non reactive NT-PRO BNP 11:-21.27 Trop I :-0.006 Ser.ferritin:-815.18 u.micro albumin:-2.00 amylase:-129 ser.ino.phosphor:-4.02 Mg:-1,41 uric acid:-4.1 blood group & rh o(+)ve positive

17. USS/CT

18. USS/CT

19. diagnosis Chronic Liver Cell Disease (CLCD) Introduction Definition: Chronic Liver Cell Disease is a progressive condition where liver cells (hepatocytes) are damaged over time, leading to fibrosis, cirrhosis, and eventual liver dysfunction. Epidemiology: Affects millions worldwide; more common in adults 40–60 years. Leading causes: chronic hepatitis B/C, alcohol abuse, non-alcoholic fatty liver disease (NAFLD). Significance: Understanding CLCD helps in early detection, preventing complications, and improving patient outcomes.

20. Etiology / Causes CLCD Viral: Chronic hepatitis B and C infections. Alcohol: Long-term excessive alcohol intake. Metabolic: Non-alcoholic fatty liver disease, Wilson’s disease, hemochromatosis. Autoimmune: Autoimmune hepatitis. Drugs / Toxins: Long-term hepatotoxic drugs, exposure to toxins

21. Pathophysiology Continuous liver cell injury Inflammation Fibrosis Cirrhosis Hepatic dysfunction.

22. Pathophysiology CLCD Hepatic encephalopathy → neurocognitive changes. Impaired protein synthesis → hypoalbuminemia, edema. e, Impaired clotting factor production → coagulopathy. Portal hypertension → ascites, splenomegaly .

23. . General Symptoms These are due to poor liver cell function and reduced metabolism: Fatigue (tiredness) Weakness Loss of appetite (anorexia) Weight loss Malaise (general feeling of illness) Skin and Eye Changes Due to buildup of bilirubin (jaundice): Yellow discoloration of skin, eyes (jaundice) Itching (pruritus) due to bile salt deposition Spider angiomas (small, star-like blood vessels on skin) Palmar erythema (red palms) Bruising easily (due to low clotting factors) Clinical Symptoms of Chronic Liver Cell Disease (CLCD)

24. . Nervous System (Hepatic Encephalopathy) Due to ammonia accumulation in the brain: Confusion or forgetfulness Behavioral changes or irritability Slurred speech Drowsiness or coma in severe cases Tremor (flapping tremor / asterixis) Gastrointestinal Symptoms Due to poor digestion and portal hypertension: (from enlarged liver or ascites) Indigestion Esophageal varices bleeding → vomiting blood (hematemesis) or black stool (melena) Clinical Symptoms of Chronic Liver Cell Disease (CLCD)

25. Abdominal Findings Due to fluid accumulation and enlarged organs: Ascites (swollen abdomen with fluid) Hepatomegaly (enlarged liver, early stage) Splenomegaly (enlarged spleen) Umbilical hernia (due to increased abdominal pressure)) Fluid and Electrolyte Imbalance Edema (swelling) in legs, ankles, feet Oliguria (decreased urine output) Hyponatremia (low sodium) Clinical Symptoms of Chronic Liver Cell Disease (CLCD)

26. Hematological Changes Anemia (pale skin, tiredness) Bleeding gums or nose Prolonged bleeding time after injury

27. Clinical Manifestations CLCD Fei Impression Design is a professional advertising design and production studio, focusing on plane, OFFICE, photography and other businesses. TITLE ZHAO FEI Fei Impression Design is a professional advertising design and production studio, focusing on plane, OFFICE, photography and other businesses. TITLE ZHAO FEI Fei Impression Design is a professional advertising design and production studio, focusing on plane, OFFICE, photography and other businesses. Jaundice , pruritus Ascites ,

28. Clinical Manifestations CLCD Fei Impression Design is a professional advertising design and production studio, focusing on plane, OFFICE, photography and other businesses. TITLE ZHAO FEI Fei Impression Design is a professional advertising design and production studio, focusing on plane, OFFICE, photography and other businesses. TITLE ZHAO FEI Fei Impression Design is a professional advertising design and production studio, focusing on plane, OFFICE, photography and other businesses. Gastrointestinal bleeding (esophageal varices) , Hepatic encephalopathy (confusion, asterixis) Easy bruising, coagulopathy ,

29. Laboratory Tests: LFTs: ↑ AST, ALT, bilirubin; ↓ albumin Coagulation profile: ↑ PT/INR Viral markers: HBsAg, anti-HCV Imaging: Ultrasound / CT: liver size, nodularity, ascites. Histology: Liver biopsy for definitive staging. Other Tests: Endoscopy for varices, elastography for fibrosis. Diagnostic Evaluation

30. Medical Management Drug Tx Common Medications: Lactulose: To reduce ammonia → prevents hepatic encephalopathy Spironolactone / Furosemide: For ascites Vitamin K: For bleeding tendency Antivirals: For hepatitis B or C Propranolol: To reduce portal hypertension

31. Medical Management Drug Tx Antivirals Tenofovir, Entecavir, Sofosbuvir + Velpatasvir Infection Risk (e.g. SBP) Cefotaxime, Ciprofloxacin (prophylaxis) Anti-inflammatory / Immune Prednisolone, Azathioprine Chelating agents Penicillamine, Trientine Supplements B-complex, Folate

32. Viral Hepatitis B Tenofovir, Entecavir, Lamivudine Viral Hepatitis C Direct-acting antivirals (DAAs): Sofosbuvir + Velpatasvir, or Ledipasvir Alcoholic Liver Disease Complete alcohol abstinence; nutritional therapy (B-complex, folate, thiamine) Autoimmune Hepatitis Corticosteroids (Prednisolone) ± Azathioprine Non-Alcoholic Fatty Liver Disease (NAFLD/NASH) Lifestyle modification, Metformin, Vitamin E Wilson’s Disease Penicillamine, Trientine Hemochromatosis Phlebotomy or Deferoxamine Medical Management Drug Tx

33. Treat the Underlying Cause The first step is always identifying and removing the cause of liver injury. Viral Hepatitis: Antiviral drugs such as Tenofovir, Entecavir, or Sofosbuvir–Velpatasvir are given to suppress viral replication and prevent further liver damage. Alcoholic Liver Disease: Complete abstinence from alcohol is essential. Nutritional supplements like thiamine, folic acid, and multivitamins are given to correct deficiencies.

34. Treat the Underlying Cause Autoimmune Hepatitis: Prednisolone (a corticosteroid) and Azathioprine are used to reduce liver inflammation. Metabolic Disorders: Wilson’s Disease: Copper chelators like Penicillamine or Trientine. Hemochromatosis: Regular phlebotomy or Deferoxamine to remove excess iron. NAFLD/NASH: Weight reduction, control of diabetes, and lipid management

35. Manage Complications Ascites: Spironolactone (first-line diuretic) ± Furosemide. Low-sodium diet and fluid restriction if severe. Paracentesis may be done for large-volume ascites. Portal Hypertension & Variceal Bleeding: Non-selective beta-blockers (Propranolol or Nadolol) reduce portal pressure. Octreotide or Vasopressin during acute variceal bleeding. Endoscopic variceal ligation (EVL) to control bleeding.

36. Manage Complications Hepatic Encephalopathy: Lactulose syrup to reduce ammonia absorption. Rifaximin or Neomycin to suppress intestinal bacteria. Dietary protein moderation if encephalopathy is severe. Coagulopathy: Vitamin K injection to correct clotting defects. Fresh frozen plasma (FFP) if bleeding occurs.

37. Manage Complications Infection (Spontaneous Bacterial Peritonitis): Broad-spectrum antibiotics like Cefotaxime or prophylaxis with Ciprofloxacin. Pruritus (Itching): Cholestyramine binds bile acids; antihistamines for relief.

38. Nutritional and Supportive Care Diet: High-calorie, moderate-protein, low-sodium diet. Vitamins: Supplementation with A, D, E, K, B-complex, and folic acid. Avoid hepatotoxic drugs: e.g. paracetamol overdose, NSAIDs. Adequate rest to reduce metabolic stress on the liver.

39. Advanced Therapy Regular follow-up with Liver Function Tests (LFTs), coagulation profile, and imaging. Screen for hepatocellular carcinoma (HCC) with ultrasound and alpha-fetoprotein (AFP) every 6 months. Liver Transplantation is the definitive treatment for end-stage CLCD when medical management fails. Pre-transplant optimization includes controlling ascites, infections, encephalopathy, and nutritional status.

40. nursing intervention

41. General condition: fatigue, jaundice, weight loss, pruritus, bleeding tendency. Vital signs : note fever (infection), tachycardia (anemia), hypotension (fluid loss) Abdominal findings: hepatomegaly, ascites, tenderness, girth measurement. Neurological status: confusion, irritability, asterixis → signs of encephalopathy. Fluid balance: intake and output, daily weight, presence of edema. Lab values: LFTs, bilirubin, PT/INR, serum ammonia, albumin. Nursing Assessment

42. Excess fluid volume related to portal hypertension and sodium retention. Risk for bleeding related to decreased clotting factors. Imbalanced nutrition: less than body requirement related to anorexia and malabsorption. Impaired skin integrity related to pruritus and edema. Disturbed thought processes related to hepatic encephalopathy. Knowledge deficit regarding disease management and lifestyle modifications. Nursing Diagnosis

43. A. Fluid and Electrolyte Balance Monitor intake/output, daily weight, and abdominal girth. → Detect early signs of fluid retention or ascites. Administer diuretics (spironolactone, furosemide) as prescribed. Restrict sodium intake and advise fluid restriction if severe ascites. Position patient in semi-Fowler’s to ease breathing in ascites. Nursing Interventions and Rationales

44. B. Prevent Bleeding Monitor for petechiae, bruising, melena, hematemesis. Avoid IM injections, rectal thermometers, and hard toothbrushes. Administer Vitamin K or FFP if ordered. Keep emergency tray ready during invasive procedures. Nursing Interventions and Rationales

45. C. Manage Hepatic Encephalopathy Observe for changes in consciousness, behavior, handwriting, speech. Give Lactulose syrup as ordered; monitor stool frequency (2–3/day). Limit protein intake if ammonia level is high. Maintain a quiet environment and ensure patient safety (side rails, assistance with ambulation). Nursing Interventions and Rationales

46. D. Promote Nutrition Small, frequent high-carbohydrate, moderate-protein meals. Vitamin and mineral supplements (B-complex, A, D, E, K, folic acid). Encourage foods the patient can tolerate; avoid alcohol and fatty foods. Nursing Interventions and Rationales

47. E. Relieve Pruritus and Maintain Skin Integrity Trim nails short; encourage cool baths and use of emollients. Cholestyramine or antihistamines as prescribed. Keep linen clean, dry, and soft. Nursing Interventions and Rationales

48. F. Prevent Infection Monitor temperature, WBC count. Practice aseptic technique for IV lines, paracentesis, or catheter care. Encourage oral hygiene and good nutrition to strengthen immunity. Nursing Interventions and Rationales

49. G. Psychological and Emotional Support Acknowledge anxiety, body-image issues (jaundice, ascites). Encourage family participation and provide reassurance. Teach relaxation or coping techniques. Nursing Interventions and Rationales

50. H. Health Education Educate on disease process, medication adherence, diet, alcohol avoidance, and regular follow-up. Explain early warning signs to report: bleeding, confusion, weight gain, jaundice worsening. Nursing Interventions and Rationales

51. Evaluation CLCD Patient maintains fluid balance and shows reduced ascites. No active bleeding or infection. Improved mental status. Adequate nutritional intake. Demonstrates understanding of long-term management.

52. Continue prescribed medications (lactulose, diuretics, antivirals). Avoid hepatotoxic drugs and alcohol. Maintain regular check-ups and vaccinations (hepatitis A & B). Family support and community health follow- up for chronic care. Discharge Planning

53. Key Takeaways CLCD CLCD is progressive but manageable with early detection. Multidisciplinary care is critical: medical, nursing, nutritional, psychological support. Nurses play a key role in monitoring, patient education, and preventing complications. Case study highlights the importance of individualized care and holistic management.

54. References WHO. Chronic liver disease facts. Kumar, V., et al. Robbins & Cotran Pathologic Basis of Disease, 10th edition. Lewis, S. Medical-Surgical Nursing, latest edition.

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