Title | CPC Case Alcoholic Liver Cirrhosis |
---|---|
Author | Rom Acc 2nd |
Course | Clinico Pathologic Conference 1 |
Institution | University of Perpetual Help System Jonelta |
Pages | 14 |
File Size | 362.1 KB |
File Type | |
Total Downloads | 23 |
Total Views | 145 |
A 75-year-old Filipino male with a chief complaint of weight loss. Two months prior to consultation, he felt progressive weakness, poor appetite with a weight loss of 15 to 20 kg. One month prior to consultation, his family noticed that at times, he exhibited disorientation to time or location and ...
UNIVERSITY OF PERPETUAL HELP SYSTEM DALTA JONELTA FOUNDATION SCHOOL OF MEDICINE CLINICO-PATHOLOGICAL CONFERENCE
October 16, 2020
I.
HISTORY AND PHYSICAL EXAMINATION History of Present Illness A 75-year-old Filipino male with a chief complaint of weight loss. Two months prior to consultation, he felt progressive weakness, poor appetite with a weight loss of 15 to 20 kg. One month prior to consultation, his family noticed that at times, he exhibited disorientation to time or location and also had difficulty recognizing close family members. As time went on, his symptoms worsened and had continued weight loss, which therefore led him to consult. He has a history of hypertension and takes 5mg OD felodipine for medication, and a history of hypothyroidism and uses levothyroxine as treatment.
Past Medical History: (+) Hypertension (+) Hypothyroidism Personal/Social History: Married, non-promiscuous Heavy drinker - Began: 15 years old - Minimum 1-2 bottles of hard liquor/5+ bottles of beer a day - 1 pack year smoker
Physical Examination General Survey: alert, responds to commands, currently oriented to time, place, person, and situation; intact recent and remote memory; warm and dry skin, slightly jaundiced; weak appearance and emaciated Vital signs: BP: 140/80 PR: 97/min reg RR: 26/min Temp: 37.8 °C HEENT: normocephalic without scalp lesions; pale conjunctiva, icteric sclerae; EOM’s full; no strabismus or nystagmus; pupils equal round, react to light and accommodation; visual fields intact to confrontation; no enlarged lymph nodes Chest/Lungs: respiratory excursions full and symmetrical; lungs resonant to percussion & vesicular breath sounds throughout peripheral lung; no rales, ronchi, wheezes, or rubs; normal vocal and tactile fremitus Cardiovascular: no abnormal heaves, lifts, thrills; regular rate and rhythm Abdomen: diffuse tenderness at the right hypochondrium; normal bowel sounds, no bruits; slightly enlarged liver edge; non-palpable spleen Extremities: intact, full, and equal distal pulses (or: femoral, popliteal, PT, and DP pulses)
Course in the Wards Day 1: Patient treated with unspecified IV antibiotics and Vitamin B supplementation Day 2: Patient’s vital signs deteriorated. Corticosteroids were given
Day 3.5: Patient’s platelet count dropped to below 7x103.. Patient went into code and was placed on ventilatory support Day 4: Patient arrested again and was not revived
II.
DIAGNOSTICS LABORATORY FINDINGS (done on admission day) Result
Reference Value
Remarks
HGB
11.3
12 – 15
LOW
Hct
0.38
0.36 – 0.45
Normal
WBC
6.0
4 – 11
Normal
Bands
16
3-5
HIGH
Seg
72
50 - 70
HIGH
Eosinophils
2
0-6
Normal
Basophils
0
0-3
Normal
Lymphocytes
26
20 - 40
Normal
Monocytes
0
2-8
LOW
Platelets
45
150 – 400
LOW
CRP
572
10 mg/L
HIGH
INR
1.48
1.0
HIGH
Serum AFP
1.21
Less than 8 ng/dL
Normal
Urea
190
5 – 25 mg/dL
HIGH
Creatinine
2.1
0.4 – 1.3 mg/dL
HIGH
K
3.7
3.5 – 5.0
Normal
Na
139
136 – 140 mEq/L
Normal
ALT
69
9 – 36 U/L
HIGH
AST
250
10 – 31 U/L
HIGH
Total Bilirubin
6.5
0.3 – 1.2 mg/dL
HIGH
Total Protein
4.83
6 – 8 g/dL
LOW
Albumin
2.5
3 – 5 g/dL
LOW
LDH
787
120 – 246
HIGH
Alk Phos
88
10 – 100 U/L
Normal
Hemoglobin A condition that affects the normal production of red blood cells. Hemoglobin levels usually mirror RBC levels, hence the decrease. Low hemoglobin could indicate a number of causes, but those pertinent to this case are the following: anemia, hypothyroidism, and cirrhosis. Neutrophil Bands and Segmenters Neutrophils make up the largest part of the circulating WBCs. These are mostly found in areas with damage or infected tissue, where they engulf mostly bacteria. The patient has neutrophilia according to the increased bands and segmenters. High neutrophil levels are indicative of bacterial infection. Monocytes Like neutrophils, monocytes travel to areas with infection and destroy bacteria. They are more commonly seen in chronic rather than acute infections. Repeated low counts of monocytes or monocytopenia can be caused by bone marrow damage or failure, bloodstream infections, or chemotherapy. Platelets Low platelet counts or thrombocytopenia could mean a number of things, one of which is the decrease in ability to clot blood. Other indications include bacterial infections, cirrhosis, and excessive alcohol drinking. C-Reactive Protein C-reactive protein or CRP is a protein produced by the liver. High levels of CRP suggests the presence of inflammation or a bacterial infection. International Normalized Ratio (INR) The international normalized ratio or INR is a calculation based on results of the prothrombin time or PT that is used to monitor individuals who are being treated with the blood-thinning medication (anticoagulant) warfarin. When the INR is higher than the recommended range, it means that your blood clots more slowly than desired. Creatinine Test Creatinine in the body is produced by muscle metabolism and minimally due to meat diet. This chemical waste product is filtered by the kidney and is excreted through the urine. In the case of an elevated serum creatinine, it means that the patient’s glomerular filtration rate has decreased and the kidney is not functioning properly. BUN Urea is generated from protein breakdown and is considered as the principal
nitrogenous waste product of metabolism. This is excreted by the kidney via Urine. In the case of the patient, elevated urea could mean that there might be an increase in the production of urea or a decrease in its elimination. There is also a possibility that it is a combination of both. Given that the patient also has an increased creatinine, it means that the glomerular filtration rate of the patient is decreased pertaining to the kidneys that are not functioning properly. Liver Function Test Testing for the LDH, Total Protein, Albumin, ALT, AST and Total Bilirubin is part of the liver function test. This test would help diagnose if the liver is damaged. Alanine Transaminase (ALT) is an enzyme that is found in the liver which helps in converting proteins to energy for the liver cells. If there is damage in the liver, this enzyme would be released into the bloodstream causing the increased levels in the liver function test. Aspartate Transaminase is an enzyme that aids in metabolizing amino acids. AST would also be increased if the liver is damaged or there is a possibility of muscle damage. Bilirubin is a product of RBC breakdown and this passes through the liver before it gets excreted in stool. An elevated may indicate that the liver is damaged. In the case of the patient, ALT, AST and Total Bilirubin are all elevated meaning the patient has a damaged liver. L-lactate dehydrogenase (LDH) is also an enzyme found in the liver and higher than normal levels indicates liver damage. Low levels of albumin and total protein also indicates liver damage. In the case of the patient, ALT, AST, Total Bilirubin and LDH are increased while Total Protein and Albumin is below normal which suggests that the liver is damaged URINALYSIS Result Color
Yellow, hazy
Specific Gravity
1.019
Urine pH
6.0
Bilirubin
Negative
Urobilinogen
0.3
Protein
1+
Glucose
Negative
Ketones
Negative
Leukocyte esterase
2+
Nitrite
Negative
RBC
Occasional
WBC
15 - 30
Epithelial cells
2-5
Bacteria
4+
Casts
Positive
Urine culture
Negative
Leukocyte esterase 2+ - Few white blood cells are normally present in urine. When the number of WBCs in urine increases significantly, this screening test will become positive. - High WBC count in the urine (leukocyturia) may indicate that there is inflammation in the urinary tract or kidneys, most commonly caused by a bacterial urinary tract infection (UTI).
High WBC (15 – 30) - WBC count in urine is normally low (0-5 WBCs per high power field, HPF). WBCs can be a contaminant, such as those from vaginal secretions. - Increased WBCs seen in the urine and/or positive test for leukocyte esterase may indicate an infection or inflammation somewhere in the urinary tract. If also seen with bacteria, they indicate a likely urinary tract infection. Bacteria 4+ - The urinary tract is sterile and, if the urine sample is collected as a "clean-catch" sample, there will be no microbes seen in the urine sediment under the microscope. - Bacteria from the surrounding skin can enter the urinary tract at the urethra and move up to the bladder, causing a urinary tract infection (UTI) Positive Casts - Presence of casts in the urine indicates a kidney disorder. When a disease process is present in the kidney, cells or other substances can become trapped in the protein as the cast is formed. SEROLOGIC TESTS Test
Result
HIV-1
Negative
Hepatitis B (HBsAg)
Negative
Hepatitis C
Negative
EBV
Negative
Blood culture
Negative
III.
DIFFERENTIAL DIAGNOSES
1. Alcoholic Liver Disease The alcoholic liver disease covers a spectrum of disorders beginning from the fatty liver, progressing at times to alcoholic hepatitis and culminating in alcoholic cirrhosis, which is the most advanced and irreversible form of liver injury related to the consumption of alcohol. There are three histologic stages of alcoholic liver disease: ● ●
●
Alcoholic Fatty Liver or Steatosis - At this stage, fat accumulates in the liver parenchyma. Alcoholic Hepatitis - Inflammation of liver cells takes place at this stage, and the outcome depends on the severity of the damage. Alcohol abstinence, nutritional support, treatment of infection, and prednisolone therapy in severe cases can help in the treatment of alcoholic hepatitis, but more severe cases lead to liver failure. Alcoholic Cirrhosis - Liver damage at this stage is irreversible and leads to complications of cirrhosis and portal hypertension.
RULE IN
RULE OUT
●
Male
●
(-) Nausea and vomiting
●
Chronic alcoholic
●
(-) Portal Hypertension: pedal edema, ascites, caput medusae
●
(+) Poor appetite and weight loss
●
(-) Yellow hazy urine
●
(+) Anorexia
●
(-) Bacteria and granular cast in the urine
●
(+) Weakness
●
(-) Hyponatremia
●
(+) Not oriented to time and location (confusion)
●
(-) Hypokalemia
●
(+) Fever
●
(+) Icteric sclerae and slightly jaundiced skin
2. Hepatocellular Carcinoma Hepatocellular carcinoma (HCC) is considered the most common primary liver malignancy and is a leading cause of cancer-related death worldwide. Chronic liver disease and cirrhosis remain the most important risk factors for the development of HCC of which viral hepatitis and excessive alcohol intake are the leading risk factors worldwide. The relationship between alcohol and liver disease correlates with the amount of alcohol consumed over a lifetime, with heavy alcohol use rather than social drinking being the main risk of HCC. RULE IN Male Age: 75 years old (+) Weight loss (+) fatigue (+) loss of appetite Diffuse tenderness on the right hypochondriac region Liver edge slightly enlarge (+) low platelet levels Heavy alcohol consumption Smoking Not oriented to time and location (+) bacteriuria Liver cirrhosis thrombocytopenia Elevated ALT
RULE OUT
Extremely elevated AST Hyperbilirubinemia Jaundice Elevated LDH
3. Hepatic Encephalopathy Hepatic Encephalopathy is a brain deterioration function which occurs secondary to severe liver disease. Substances absorbed into the bloodstream from the intestine pass through the liver, where toxins are normally removed. Many of these toxins (such as ammonia) are normal breakdown products of the digestion of protein. In hepatic encephalopathy, toxins are not removed because liver function is impaired ammonia then crosses the blood brain barrier which results in neurologic symptoms. RULE IN
RULE OUT
●
Disorientation
●
(-) Asterixis
●
Short term memory loss
●
(-) Hyperreactive reflexes
●
Liver Cirrhosis
●
Undetermined Ammonia Levels
●
Elevated Liver Enzymes
●
Elevated LDH
●
Decreased albumin level
●
(+) Murphy’s Sign ; Hepatomegaly
●
(+) Jaundice
●
(+) Icteric Sclera
●
Chronic Alcoholic
●
Decreased appetite
●
Rapid breathing (RR=26)
4. Hepatorenal syndrome(HRS) Hepatorenal syndrome develops spontaneously in patients with advanced cirrhosis who have no objective criteria for a precipitating event other than progressive liver failure. Although HRS occurs predominantly in advanced cirrhosis, it may also develop in other
chronic liver diseases associated with severe liver failure and portal hypertension, such as alcoholic hepatitis or acute liver failure. The cirrhosis is most commonly a result of infectious hepatitis or chronic alcoholism. Azotemia, hyponatremia, oliguria, low urinary sodium concentration are typical features. Without treatment, the median survival for type 1 hepatorenal syndrome patients is on the order of 1–2 weeks, while that for type 2 hepatorenal syndrome is about 20% at 1 year. Also, it must be emphasized that urinary parameters are supportive, but not essential for the diagnosis of hepatorenal syndrome.
RULE IN
RULE OUT
Liver cirrhosis
Presence of ascites (Undetermined)
Jaundice
(-) Muscle jerks
Altered mental status (at times not oriented to time or location, or had difficulty remembering close family members.)
(-) Oliguria
Renal failure
(-) Hyponatremia
Azotemia (Elevated BUN and creatinine)
5. Acute Suppurative Cholangitis Acute suppurative cholangitis has a classic manifestation of a clinical pentad symptoms of fever, jaundice, pain, shock and central nervous system depression. This disease represents a true surgical emergency. In suppurative cholangitis, the obstruction becomes complete, and ductal pressure rises rapidly as the bacteria present in bile proliferate. When the ductal pressure achieves a critical level, above the secretory pressure of the liver, bacteria and endotoxins are forced into the systemic circulation by way of the hepatic sinusoids, producing a fulminant course of overwhelming bacteremia and sepsis. RULE IN
RULE OUT
Fever
(-) Leukocytosis or leukopenia
Jaundice
Alkaline Phosphatase within normal range
Icteric sclerae
Blood culture - negative
Altered mental status (not oriented to time or location)
Rapid weight loss
Tenderness at the right hypochondrium
(-) Weakness
Hepatomegaly
(-) Shock (BP: 140/80mmHg)
Elevated AST Extremely elevated ALT Thrombocytopenia Hypoalbuminemia Hyperbilirubinemia Chronic alcoholic
6. Spontaneous bacterial peritonitis secondary to liver cirrhosis Spontaneous bacterial peritonitis (SBP) is one of the most common and lifethreatening complications of cirrhosis. It is the infection of fluid from ascites without a source of intra-abdominal infection such as intra-abdominal abscesses, intestinal perforation, and in the absence of intra-abdominal inflammation such as cholecystitis or acute pancreatitis. In this case, there is no pertinent finding in CBC that could be associated with SBP however, it should be noted that the diagnostic standard for SBP is PMN count in ascitic fluid/paracentesis. Urine strip test has also been used as a rapid diagnostic in some studies where pertinent finding is presence of leukocyte esterase which is present in our patient (2+ leukocyte esterase). The aforementioned conditions are the reasons for ruling this in. However, it is crucial to establish first that the patient has ascites. Other than the diffused tenderness in the abdomen particularly in the right hypochondrium, no other associated symptoms that could suggest ascites were noted such as weight gain, abdominal pain and distention. RULE IN Liver cirrhosis thrombocytopenia Elevated ALT Extremely elevated AST Hyperbilirubinemia Jaundice Elevated LDH Spontaneous bacterial peritonitis Fever Encephalopathy Renal failure - elevated urea, creatinine, decreased albumin in patient Elevated INR Elevated CRP Leukocyte esterase
RULE OUT
Presence of ascites not established (+) weight loss (-) abdominal distention (-) abdominal pain
7. Autoimmune Hepatic Anemia: Warm Antibody Hemolytic Anemia Autoimmune hepatic anemia is characterized by the breakdown of RBCs (with or without complement activation). Hepatic failure ensues because of the warm-reacting IgM antibodies through in vivo auto agglutination. In some cases, AIHA also presents as acute liver failure.
RULE IN
RULE OUT
Elevated levels of LDH
Non Palpable spleen
Total bilirubin exceeds 5 mg/dL
Non diarrheic
Increased AST level (>30)
(+) eosinophilia
Elevated CRP
Normal RBCs
Elevated creatinine
V.
FINAL DIAGNOSIS AND PATHOPHYSIOLOGY
Working Diagnosis: Liver Cirrhosis
Liver Insufficiency The patient’s chronic consumption of alcohol led to the hepatic impairment possibly due to fatty liver which is the most common histologic response to hepatotoxic stimuli which is excessive alcohol ingestion. These series of insults to the liver eventually led to liver cirrhosis as manifested in the patient’s signs and symptoms (weight loss, weakness, and hepatomegaly) and lab findings like elevated AST and ALT. Since there is a presence of chronic regeneration due to having chronic cirrhotic liver, it might as well subsequently lead to formation of hepatocellular carcinoma.
Upon admission, the patient ...