SPONTANEOUS

BACTERIAL
PERITONITIS
Marion Mae Pernia MD
Level II IM Resident
 OBJECTIVES

1.To present a case of a 65 Male presents with increased in abdominal

girth
2.Review causes of ascites , diagnostic approach in patients with ascites
3.To discuss the pathophysiology of Spontaneous Bacterial Peritonitis,
Risk factors , diagnosis and treatment
CASE
M.J
• 65
• Male
• No known co-morbidities
• Resides at Quezon City
 HISTORY OF PRESENT ILLNESS
Temporal Profile
Increased
abdominal girth

Early satiety

Loss of appetite

vomiting

Difficulty of Consult
breathing

2 weeks 1 week 1 day

1 month
 Personal & Social
(-) Hypertension History
Past Medical
(-) DM
History (-) PTB (+) 3 pack year smoker
(+) Alcoholic beverage drinker x 11 years (7
(-) Bronchial Asthma standard drink of beer everyday)
(-) Kidney Disease Denies illicit drug use
Jeepney driver

Family Medical Sexual History

(+) DM - both
History (+) Hypertension - father 3 sexual female partners
(-) PTB Protected
(-) Liver Disease
(-) Kidney Disease
(-) Malignancy No Travel History
 Review of Systems

(+) weight loss- undocumented

(-) changes in bowel habits
(-) melena/hematochiezia
(-) dec in caliber of stool
(-) PND
(-) edema
(-) easy fatigability
(-) blurring of vision
(-) syncope
(-) palpitations
(-) hot/cold intolerance
 PHYSICAL EXAMINATION
General Survey
Head and Neck
Icteric sclerae, Slightly Palpebral
Conjuctivae,(-) nasoaural discharge
(-) Cervicolymphadenopathy
(+) dry lips and mucosa
Cardiovascular
Adynamic precordium, tachycardic, regular
rhythm, (-) murmur PMI not displaced
Abdomen
Globular abdomen ,Abdominal girth:90cm, Liver
span: 9 cm everted umbilicus with no visible
engorged veins, hypoactive bowel sounds, no
palpable mass, warm to touch, non tender (+)
shifting dullness , Traube’s space obliterated
upon percussion
Medium built, Cachiectic, BMI: 17.5 AG:90
BP: 100/70 HR: 104 RR: 25cpm T:37.9C O2sat: 96% at room air
Awake, coherent, in mild distress
Chest and Lungs
Symmetrical Chest Expansion, (-)
Retractions (-) Lagging , VBS
Extremities
Grossly normal extremities,(+) spider angiomas on
upper extremities (-) palmar erythema (-) asterixis (-)
gynecomastia (-) cyanosis (-) edema
Digital Rectal Examination
No skin tags, hemmorhoids, fissures.
External sphincter tone intact. Rectal vault without
masses. Prostate gland is smooth, nontender. Fecal
material is non-bloody on tactating finger
 NEURO PE
GCS 14 (E4V4M6) Motor: 5/5 on right upper and lower extremities and left
Frontal: Awake, alert, good speech, poor insight and judgment upper extremities;
Temporal: unable to assess immediate, recent, and remote 5/5 on left lower extremities; with limited range of motion on
memory left lower extremities
Occipital: Able to identify 3 objects and 3 colors
Parietal: No right-left disorientation, no apraxia, agraphesthesia, Sensory: 100% on right extremities and left upper
finger agnosia extremities; 100% on left lower extremities (L1-L5
distribution); No Romberg’s sign
CN I: N/A
CN II, III: Pupils 3mm equally brisk and reactive to light; intact visual Muscle-Stretch Reflexes: +2 Bilateral upper and lower
fields; (+) ROR extremities
CN III, IV, VI: primary gaze midline, no ptosis, intact extraocular
muscles Pathologic reflexes: no Babinski
CN V: intact facial sensory; good masseter and temporalis tone
CN VII: no facial asymmetry Cerebellar: no dysmetria, dysdiadochokinesia,
CN VIII: intact gross hearing;
CN IX, X: uvula midline, intact gag reflex Meninges: supple neck, no nuchal rigidity, No Brudzinski, No
CN XI: good shoulder shrug on left, unable to shrug shoulder on Kernig’s sign
right
CN XII: tongue deviated to right, no atrophy, no fasciculations
 SALIENT FEATURES
• Male
• 65 years old
• No known co-morbidities
• Increased in abdominal girth
• Loss of appetite
• Early satiety
• 2 episodes of Nausea/vomiting
• Difficulty of breathing
• Difficulty in sleeping
• ROS: (+)undocumented weight loss
(-) abdominal pain (-)
melena/hematochieza (-) changes in
bowel habits (-)
• 3 year pack year smoker
• Alcoholic beverage drinker x 11 years
(7 standard drink of beer everyday)
• Denies illicit drug use
• 3 sexual female partners, protected
• No travel history
• BMI: 17.5 Abdominal Girth:90cm
• Icteric sclerae (+) Jaundice slightly pale
palpebral conjuctivae
• Tachycardic
• Globular abdomen , Liver span:9 cm
everted umbilicus with no visible engorged veins,
hypoactive bowel sounds, (-) palpable mass, (+)
warm to touch (+) shifting dullness
• (+) spider angiomas on upper extremities (-)
palmar erythema (-) asterixis (-) gynecomastia
(-) cyanosis (+)grade I bipedal edema
 WORKING IMPRESSION
Decompensated Liver Cirrhosis probably secondary
Alcoholic Liver Disease
To consider Spontaneous Bacterial Peritonitis
COVID suspect
Complete Blood Count
WBC 19.90
Normal
Values Bleeding Parameters
BUN 5.53 2.14-
7.14 PT 24.1 11-18 secs
RBC 6.71
Crea 67.51 62-106
Na 130.5 135-155 PTT 44.1 24.0-39.0
Hgb 107 secs
K 2.90 3.4. - 5.3
HCT 25.1 INR 1.47 0.81-1.37
AST 152.4 (3.8x) 0-40 U/L

MCV 90.2 ALT 109.10 (2.7x) 0-40 U/L

MCH 29.1 LDH 237 (1.1x) TPAG

MCHC 319 ALP 140 40-130 Total Protein 57.67

Plt 105 Total 39.0 (1.8x) 0-21 Albumin 20.27

Bilirubin
Neu 84.2 Direct 43 0-5.0 Globulin 37.40
Lymph 34.8 Bilirubin
Indirect 37.23 HbsAg Non-reactive
Bilirubin
Mono 3.2
Anti-HCV Non-reactive
Eos 0.1 Anti - HBc Non-reactive

Baso 0.4 Clinical Chemistry HBeAg Non-reactive

Anti HBe -
1.Cirrhosis with signs of portal hypertension (Portocaval varices,
splenomegaly•andThe liver is small in size measuring 10.2 cm in its midhepatic length
moderate
and
ascites)
exhibits inhomogenous parenchyma with widened periportal and
No evidence of enhancing mass
interlobar lesion.
space. The left lobe extends laterally to contact the
spleen.
2. Simple hepatic cyst (1.1cm) in segment VIL
3. Cholelithiasis and gallbladder sludge
• Prominent esophageal, gastric, perisplenic, mesenteric and
paraumbilical collaterals.
• Contrast enhancement of the paraumbilical vein is appreciated.
ASCITES
 ABDOMINAL PARACENTESIS
documented no deaths or infections caused by the paracentesis
• Abdominal paracentesis with appropriate ascitic fluid analysis
is probably the most rapid and cost-effective method of
diagnosing the cause of ascites.
Complications were reported in only about 1% of patients (abdominal wall
hematomas), despite the fact that 71% of the patients had an abnormal prothrombin
• The analysis of ascitic fluid is essential for detecting ascitic
time

fluid infection and excluding causes of ascites other than

Although
cirrhosis, in more
casesserious complications
in which the (hemoperitoneum
diagnosis is or bowel
not entry by the
clear
paracentesis needle) occur they are sufficiently unusual (<1 /1000 paracetesis)
that they should not deter performance of this procedure

Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
 PARACENTESIS

If the fluid is difficult to localize

by examination because of
1 or 1.5 inch 21 or 22 obesity, ultrasonography can be
gauge needle: Lean a useful adjunct in locating fluid
Patients and visualizing the spleen and
3.5 inch 22 gauge other structures to be avoided.
needle : Obese

Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
At Ward ASCITIC FLUID ANALYSIS:

COLOR: SERUM TPAG:

YELLOW
TOTAL PROTEIN ALBUMIN
ASCITIC TOTAL
TRANSPARENCY: PROTEIN
48.80 g/L 20.47 g/L
HAZY <7.60 g/L

CELL COUNT GLOBULIN A/G RATIO

RBC : 0.0 ASCITIC ALBUMIN
30.54 g/L 0.66 g/L
WBC:273/uL <4.00 g/L

DIFFERENTIAL COUNT
Segmenters: 80%
Lymphocytes: 10%
Monocytes:10%
Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
 ASCITIC FLUID ANALYSIS:
• CELL COUNT
• Single most helpful ascitic fluid test.
• Only approximately 10 μL of fluid is
required for a standard manual
hemocytometer count.
• SBP is the most common cause of
inflammation of ascitic fluid and the
most common cause of an elevated
ascitic WBC count
• TOTAL PROTEIN
• Ascitic fluid total protein concentration
DOES NOT INCREASE DURING SBP; it
remains stable before, during, and after
infection.
• Patients with the lowest ascitic protein
concentrations are the most susceptible
to spontaneous peritonitis
 ASCITIC FLUID ANALYSIS:

CULTURE
• Culture of the fluid will be highly helpful for guiding treatment if ascitic fluid
infection is confirmed.
• Ascitic fluid culture should be performed by inoculating at least 10 mL of
ascitic fluid into blood culture bottles immediately after paracentesis.
• The most common cause of ascitic fluid infection is SBP, and, in that case,
culture is expected to be monomicrobial.
 SERUM ASCITES ALBUMIN GRADIENT

• A sensitive and specific measurement to determine whether ascites is

related to portal hypertension
• The SAAG does not confirm the diagnosis of the cause of ascites but is an
indirect and accurate index of portal hypertension
• The SAAG may be useful when the cause of ascites is not clear after the
initial medical history, physical examination, standard blood tests, and
abdominal ultrasound
SERUM ASCITES ALBUMIN GRADIENT

SAAG : SERUM ALBUMIN – ASCITIC FLUID

ANALYSIS
SAAG >1.1g/dl SAAG <1.1g/dl
(11g/L) (11g/L)

Predicts that the patient has indicates that the patient

SAAG : 20.47g/L–
portal hypertension with 97% 4g/L ~ 16.4 g/L ordoes
1.64g/dl
not have portal
accuracy hypertension
 ASCITIC FLUID ANALYSIS

GRAM
STAIN
AFB

Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
PERITONITI
S • is a life-threatening event that is often
accompanied by bacteremia and sepsis

• either primary (without an apparent source of

contamination) or secondary
 SPONTANEOUS BACTERIAL
PERITONITIS
An ascitic fluid infection without an evident
intra-abdominal surgically treatable source

• It primarily occurs in patients with advanced cirrhosis

• Should be suspected in patients with cirrhosis who develop signs and

symptoms such as fever, abdominal pain, altered mental status,
abdominal tenderness, or hypotension

SPONTANEOUS BACTERIAL
PERITONITIS
Reference: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease 11th edition
 SPONTANEOUS ASCITIC
INFECTION
• Ascitic fluid infection can be classified into 5 categories:

1. ascitic culture results

2. PMN count
3. Presence or absence of a surgical source of infection

SPONTANEOUS BACTERIAL
PERITONITIS
Reference: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease 11th edition
 SPONTANEOUS
PATHOGENESIS
BACTERIAL PERITONITIS
• involve hematogenous spread of organisms in a patient in whom a
diseased liver and altered portal circulation result in a defect in the usual
filtration function.

• Proteins of the complement cascade are found in peritoneal fluid, with

lower levels in cirrhotic patients than in patients with ascites of other
etiologies

• The opsonic and phagocytic properties of PMNs are diminished in patients

with advanced liver disease.
SPONTANEOUS BACTERIAL
PERITONITIS
Small-intestinal bacterial overgrowth is frequently present in advanced stages of liver
cirrhosis and has been linked with pathologic bacterial translocation and PBP

Factors promoting these changes in cirrhosis may include deficiencies in Paneth cell
defensins, reduced intestinal motility, decreased pancreatobiliary secretions, and
portal-hypertensive enteropathy
CLINICAL MANIFESTATIONS
DIAGNOSIS
The diagnosis of spontaneous bacterial peritonitis (SBP) is made in the presence of an
elevated ascitic fluid absolute polymorphonuclear leukocyte (PMN) count (i.e., ≥250
cells/mm3 [0.25 x 109 /L]) without an evident intra-abdominal, surgically treatable
source of infection

Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012

“clinical diagnosis” of infected ascitic fluid without a paracentesis is NOT adequate; the
clinician’s clinical impression that infection is unlikely does not rule out infection

Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
 TREATMEN
T

Reference: Harrisons Principles of Internal Medicine 20th edition

 TREATMENT

Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
 DURATION OF TREATMENT

Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
 PRIMARY
• gastric acid suppression may increase the risk of
PBP
• No prospective studies have yet addressed
whether avoidance of such therapy may prevent
PBP
• A 7-day course of antibiotic prophylaxis is
recommended for patients with cirrhosis and
gastrointestinal bleeding
Reference: AASLD PRACTICE GUIDELINE Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
SECONDARY
•
PREVENTI
Antibiotic prophylaxis is recommended for
to <20% and improve short-termON
patients with a history of PBP to reduce this rate
survival rates
• Prophylactic regimens for adults with normal
renal function include fluoroquinolones
(ciprofloxacin, 500 mg weekly; or norfloxacin
[not available in the United States], 400 mg/d)
or trimethoprim-sulfamethoxazole (one double-
strength tablet daily).
 Rifaximin has been proposed as a
potential alternative prophylactic
treatment :1200 mg daily
 Resources:
● Harrisons Principles of Internal Medicine 20th edition
● Sleisenger and Fordtran’s Gastrointestinal and Liver Disease 11 th
● AASLD PRACTICE GUIDELINE Management of Adult Patients with
Ascites Due to Cirrhosis: Update 2012
 THANKS!
HAVE A GOOD DAY AHEAD!