Download Date: 30/3/2011

MEDICINE ROTATION
WEEK 8
Student Name:
Student ID:
MUBARAK HOSPITAL
Date:
31/10/2012
1
Personal Details
Name:
Mr. N.A
Age:
53 years
Marital status:
Married
Occupation:
Secretary
Residence:
Flat, 2nd floor, no elevator
Ethnicity:
Egyptian, Muslim
Presenting Complaint
3 days H/O
1) Generalized abdominal pain and distention
2) Nausea
3) Fever
4) Diarrhea
History of Presenting Complaint
MR. N.A, a known case of HCV with chronic decompensated liver cirrhosis, is a 53 years old Egyptian
gentleman who presented to the Casuality Department on 29/10/2012 with a 3 days history of abdominal
pain and distention, nausea, diarrhea and fever. The abdominal pain was sudden in onset, progressive and
continuous in nature, diffuse, colicky in character and non-radiating. It was rated as 10 in terms of
severity on a scale of 1-10. There were no aggravating or relieving factors. Concerning the fever, it was
intermittent, high grade (up to 39) and associated with chills and rigors. As for the diarrhea, the stool was
noted to be watery, non-fatty, non-bloody, and with no mucus or discharge. Associated symptoms were
anorexia and loss of appetite otherwise the patient gave no H/O vomiting, constipation, hematemesis,
dyspepsia, dysphagia, weight loss, drowsiness, cough, dysuria or hematuria.Upon further questioning, the
patient revealed H/O stopping his medications (aldactone) because of not feeling well. The patient is
known to have DM type 2 and is on treatment (insulin) with no micro or macro-vascular complications.
Past Medical History
H/O HCV+ decompensated chronic liver disease– 10 years, on aldactone 50 mg PO OD, follows up with
gastroenterologist in Egypt.
H/O DM Type 2- 7 years, compliant on insulin mixtard 80 units/day, follows up in Egypt.
No H/O HTN
No H/O hyperlipidemia
No H/O asthma
No H/O cardiac disease or other significant illnesses
No H/O past surgeries/ procedures
No H/O previous hospitalizations/ICU admissions.
2
Family History
Father
Passed away; no significant medical history
Mother
Passed away; no significant medical history
Siblings
2 brothers, 3 sisters all alive and well.
Children
3 children, alive and well.
Family
No significant illness in family
No H/O condition similar to patient’s condition
Drug History
Aldactone 50 mg PO OD
Losec 20 mg PO OD
Insulin mixtard 80 units/day
Social History
Tobacco:
Non-smoker
Alcohol:
Non-ethanol consumer
Life style:
Sedentary, lives with his family.
Stress:
None.
Travel:
No history of recent travel.
Pets:
None.
General Health Status
Appetite:
Decreased
Weight:
80 kg, constant.
Height:
175 cm.
Bowel habit:
Mentioned above.
Micturation:
Regular, no obstructive/irritative urinary symptoms, no haematuria, light yellow urine.
Sleep:
Normal.
Energy:
Decreased
Well being:
Unsatisfactory
3
Systems Review
Alimentary
Mentioned above
Respiratory
No H/O, cough, wheeze, haemoptysis, night sweats, or fatigue
Cardiovascular No H/O palpitations, syncope, orthopnea, paroxysmal nocturnal dyspnea
Urogenital
Normal stream and frequency, no H/O urgency, hesitancy, dysuria, intermittency,
hematuria, or post-micturation dribble
Joints/muscles No limitation, painful movement, swelling, joint deformities or stiffness
Neurological
No H/O drowsiness, numbness, tingling , syncope, seizures, headaches, balance and
coordination normal, no dizziness or vertigo
Special Senses: Normal hearing, normal vision, normal smell, normal tasting.
Physical Examination
The patient was alert, cooperative, responsive, well oriented to time, place and person, and lying down
comfortably in bed.
Vital Signs





Heart Rate:
Blood pressure:
Respiratory:
Temperature:
SpO2:
80/min
124/80 mmHg
15 /min
37.4 oC
98%
General Inspection
General
Normal, not in respiratory distress (no use of accessory muscles of breathing)
Hands
Palmar erythema otherwise no evidence of color abnormality like peripheral cyanosis
/tobacco staining, no nail abnormality like clubbing/ koilonychias/leukonychia/splinter
hemorrhage, no joint abnormality, no hand deformity like ulnar deviation/dupuyten’s
contracture, no muscle wasting, flapping tremor or bounding pulse,Normal Temp. of both
hands (RT=LT).
Eyes:
Conjuctival pallor and scleral jaundice
Mouth:
No evidence of mucosal cyanosis, no evidence of oral ulceration, patient has normal
teeth, no evidence of tongue abnormality like wasting/enlargement/
inflammation/discoloration/abnormal movements.
Neck
Spider nevi – otherwise no evidence of distended neck veins or parotid gland
enlargement
Muscles/joints No swelling or deformities, no evidence of erythema, or rash
4
Alimentary System
Inspection:
Hands: Palmar erythema, otherwise no clubbing, duputeryns contracture, muscle
wasting or flapping tremor.
Eyes: Jaundice and pallor, no xanthelasmas
Mouth: Clean mouth, normal breath.
Neck: 2 spider nevi, otherwise no dilated veins or parotid gland enlargement.
Chest: Gynecomastia, spider nevi >4, otherwise no dilated veins and chest moves
symmetrically with respiration
Abdomen: Abdomen is distended, umbilicus is everted, visible dilated vein, hair
loss, otherwise no scars or stomas on abdominall wall, no rashes, striae or
bruising.
Leg: No lower limb edema.
Palpation:
Abdomen is distended
Superficial palpation: Minimal tenderness, no guarding or rigidity
Deep palpation: No masses or organomegaly felt.
Liver span: Normal -10 cm
Spleen: Palpable spleen
Shifting dullness positive
Fluid thrill negative
Auscultation:
Positive bowel sounds, no bruits heard over liver or aorta.
Auscultation of chest: normal breath sounds over both lung fields, no added
sounds
Hernia:
None detected in groin, scrotum or central abdomen.
Rectal exam:
Not performed.
Respiratory System
Trachea:
Central.
Inspection:
Normal chest shape, symmetrical, elliptical in cross section, no evidence of any
deformities like kyphosis/scoliosis/pectus carinatum/ pectus excavatum, no
evidence of scars, swellings, subcutaneous lesions or dilated veins on chest wall.
Percussion:
Resonance over both lung fields (Right = Left).
Auscultation:
Vesicular breath sounds over both lung fields, no added sounds.
Chest expansion:
Normal and symmetrical expansion.
5
Cardiovascular system
Inspection of chest wall: No scars, obvious veins, bony deformities or obvious pulsations.
Radial pulse:
Normal volume, regular rhythm, normal character, symmetrical, non-collapsing.
Apex:
Palpable in the 5th ICS, within the MCL.
Auscultation:
Normal S1 and S2, no evidence of S3 orS4, added sounds or murmurs.
JVP:
Not visible.
Pulses:
Site
Right
Left
Carotid
++
++
Radial
++
++
Brachial
++
++
Femoral
++
++
Popliteal
+
+
Dorsalis Pedis
+
+
Posterior tibial
+
+
No radiofemoral delay.
Auscultation
Abdomen: No bruits heard.
Femoral: No bruits heard.
Inspection of abdomen:
No visible pulsation.
Palpation of abdomen:
Abdominal aorta not palpable.
Inspection of right leg:
rashes.
Normal hair distribution, no ischemic changes, ulcers, swelling, scars or
Palpation of right leg:
No tenderness, pitting oedema or palpable popliteal artery.
Temperature:
Normal.
Neurological System
Cranial nerves:
I – IX, XI and XII tested – normal, visual fields normal.
Reflexes:
Normal and symmetrical in both sides.
Planter reflex:
Negative.
Sensation:
Normal and symmetrical in both sides.
Motor:
Normal and symmetrical in both sides.
Power:
Normal and symmetrical in both sides.
6
Renal system
Inspection:
No abdominal distention, suprapubic swelling or scars.
Palpation:
No enlargement of kidneys/bladder or tenderness.
Ballottement:
Kidneys not enlarged.
Pressure on renal angle:
No tenderness.
Percussion over suprapubic area: Resonance.
Auscultation:
No bruits heard.
Musculoskeletal
Inspection
No evidence of swelling, erythema, rash or visible deformities
Palpation
No pitting edema, change in temperature, tenderness, or effusion detected
Movements
No restriction in movement
Lymph node examination
Cervical, axillary and inguinal LNs examined bilaterally – NAD.
Neck examination
No swellings, masses or deformities were inspected or palpated.
Investigations
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
CBC
Clinical Chemistry
Lipid Profile
Mineral Profile
Blood film
Coagulation profile
ECG
CXR
US abdomen and pelvis
αFP
Blood C/S
Ascitic tap
a. WBC & Differential
b. Gram stain
c. C/S
d. Albumin
e. Cytology
13. Serum albumin
14. HbA1C
15. 24 hour urine protein
7
16. Fundoscopy
17. UCnI endoscopy
1) CBC
Test
Result
Hb
138
N
130-170 g/L
RBC
4.07
L
4.5-5.5 x10^12/L
Hematocrit
0.412
N
0.4-0.5 L/L
MCV
99.0
N
83-101 fL
MCH
33.9
H
27-32 pg
RDW
17.9
H
11.6-14 %
Platelet count
35
LL
150-410 x10^9/L
WBC
15.9
H
4-10 x10^9/L
Neutrophils
8.3
H
1.7-7.5
Lymphocytes
0.7
L
1-3
Monocytes
0.7
N
0.2-1
Eosinophils
0.0
L
0.02-0.5
Basophils
0.0
L
0.02-0.1


Normal value
Evidence of low platelet count indicating thrombocytopenia possibly due to liver cirrhosis.
Evidence of leukocytosis mainly Neutrophils indicating underlying bacterial infection
2) Clinical Chemistry
Test
Result
Normal value
Gluc
7.2
H
3.9-6.1 mmol/L
BUN
3.4
N
2.5-7.1 mmol/L
Urea
3.4
N
1.5-6.6 mmol/L
Creat
67
N
62-115 umol/L
Na
136 N
136-144 mmol/L
K
4.3
N
3.6-5.1 mmol/L
CO2
28
N
22-32 mmol/L
Albumin
32.0
L
35-47 g/L
Cl
104
N
94-115 mmol/L
LDH
162
N
90-180 IU/L
Alk. Pho
140
H
26-88 IU/L
ALT
17
N
10-60 IU/L
AST
18
N
10-42 IU/L
8
GGT

35
N
7-64 IU/L
Evidence of slightly low albumin suggestive of underlying chronic disease or malnutrition.
1) Blood C/S
Awaiting results.
2) Sputum C/S
Awaiting results.
3) ESR/CRP
Test
Result
Normal value
ESR
14 N
0-20 m/hr
4) Urine R/M C/S
Awaiting results
5) ABG
Test
Result
Normal value
pH
7.351
7.35 – 7.45
PO2
11.78 kPa
10.67 – 13.33 kPa
PCO2
5.74 kPa
4.67 – 6.00 kPa
HCO3-
24.0 mmol/L
24 – 26 mmol/L
Normal
6) CXR
Hetereogenous opacity over right upper lobe suggestive of right lobar pneumonia
7) ECG
9
Working Diagnosis and Management Plan
From the patient's history and clinical examination of the chest, a diagnosis of Spontaneous Bacterial
Peritonitis in a case of chronic decompensated liver disease was made.
A management plan was set up for the patient and the patient was managed accordingly with:
1. Close observation of vital signs
2. Order the following investigations:
a.
b.
c.
d.
e.
f.
g.
h.
i.
j.
k.
l.
CBC
Clinical Chemistry
Lipid Profile
Mineral Profile
Blood film
Coagulation profile
ECG
CXR
US abdomen and pelvis
αFP
Blood C/S
Ascitic tap
i. WBC & Differential
ii. Gram stain
iii. C/S
iv. Albumin
v. Cytology
m. Serum albumin
n. HbA1C
o. 24 hour urine protein
p. Fundoscopy
q. UCnI endoscopy
3. Low salt, diabetic diet
4. Administer:
a. Aldactone 50 mg PO OD
b. Losec 20 mg PO OD
c. Claferan 1 gm IV TDS
d. Insulin actrapid 8 8 8
e. NPH 10 10
Based on the results of the investigations (mentioned above) of a diagnosis of Spontaneous Bacterial
Peritonitis in a case of chronic decompensated liver disease was made.
10
Summary-in-the-box
Spontaneous bacterial peritonitis (SBP) is the development of peritonitis (infection in the
abdominal cavity) despite the absence of an obvious source for the infection.[1] It occurs almost
exclusively in people with portal hypertension (increased pressure over the portal vein), usually
as a result of cirrhosis of the liver.[1] It can also occur in patients with nephrotic syndrome.
Symptoms include fevers, chills, nausea, vomiting, abdominal tenderness and general malaise.[1]
Patients may complain of abdominal pain and worsening ascites.[1] Thirteen percent of patients
have no signs or symptoms.[5] Hepatic encephalopathy may be the only manifestation of SBP; in
the absence of a clear precipitant for the encephalopathy, all patients should undergo
paracentesis, or sampling of the ascites fluid, in order to assess for SBP. SBP is thought to result
from a combination of factors inherent in cirrhosis and ascites, such as prolonged bacteremia
secondary to compromised host defenses, intrahepatic shunting of colonized blood, and defective
bactericidal activity within the ascitic fluid.[6] Contrary to earlier theories, transmucosal
migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role
in the etiology of SBP.[7]With respect to compromised host defenses, patients with severe acute
or chronic liver disease are often deficient in complement and may also have malfunctioning of
the neutrophilic and reticuloendothelial systems.[8]As for the significance of ascitic fluid
proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1
g/dL were 10 times more likely to develop SBP than individuals with higher concentrations.[9] It
is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the
protein concentration.[10] Additional studies have confirmed the validity of the ascitic fluid
protein concentration as the best predictor of the first episode of SBP.[
Diagnosis necessitates paracentesis (needle drainage of the ascitic fluid) and laboratory
confirmation of ascitic neutrophils > 250/mm³.
After confirmation of SBP, patients need hospital admission for intravenous antibiotics (most
often cefotaxime 2g IV Q8-12H for at least 5 days or ceftriaxone 2g IV Q24H). They will often
also receive intravenous albumin. A repeat paracentesis in 48 hours is sometimes performed to
ensure control of infection. Once patients have recovered from SBP, they require regular
prophylactic antibiotics as long as they still have ascites.A randomized controlled trial found that
intravenous albumin on the day of admission and on hospital day 3 can reduce renal
impairment.[11]
My references:
Davidson's principles and practice of medicine, 21st edition.
Oxford clinical medicine, 7th edition.
11