​Kembara Xtra - Medicine - Acute Peritonitis

​Kembara Xtra - Medicine - Acute Peritonitis 
Inflammation of the peritoneum is described.
A classification:
- Aseptic: systemic peritoneal inflammation or chemical irritation
Bacterial peritonitis comes in a variety of forms, including:
Infection of ascitic fluid without an intraabdominal cause is known as primary/spontaneous bacterial peritonitis (SBP).
Infection of ascitic fluid from an identifiable intra-abdominal source is the definition of secondary bacterial peritonitis. This condition can be further divided into perforation peritonitis and nonperforation peritonitis.
Third-degree bacterial peritonitis Peritoneal dialysis-associated peritonitis: >48 hours of infection despite source control The most frequent causes of acute peritonitis in children are perforated appendicitis and chronic peritoneal dialysis.

Prevention Incidence
The annual incidence of SBP in cirrhotic individuals with ascites ranges from 10 to 25 percent.
 25-75% of patients who develop tertiary peritonitis from secondary bacterial peritonitis.
Prevalence
SBP: SBP is present in about 4% of outpatients with cirrhosis and ascites who are asymptomatic. The no-show rate is 10%.
5% of peritonitis in patients with cirrhosis and ascites is secondary.
The most frequent cause of sepsis in surgical ICU patients is secondary peritonitis, and PD peritonitis is the main driver behind the move to hemodialysis (HD).
PD peritonitis affects youngsters more frequently than it does adults.

Pathophysiology and Etiology 
Bacterial translocation via lymphatic dissemination through mesenteric lymph nodes is the mechanism for SBP.
 Often appears in patients with severe cirrhosis and large-volume ascites.
Patients with cirrhosis have:
 Changes in gut microbiota that are associated with a higher prevalence of pathogenic organisms
Increased intestinal mucosal permeability to microorganisms and small intestinal bacterial overgrowth (SIBO)
 Reduced cellular and humoral immunity restricts the removal of peritoneal microorganisms.
- Subsidiary:
 Bacteria introduced through instrumentation or translocated from inflamed or punctured intraperitoneal (IP) organs
PD peritonitis is tertiary and develops from secondary peritonitis.
 Exit-site infections or contact with infectious skin bacteria during exchanges
SBP for microbiology. Over 90% of SBP cases are monomicrobial.
The most prevalent gram-negative pathogens are Klebsiella spp. (8%) and Escherichia coli (33%) respectively.
The two most prevalent gram-positive pathogens are Staphylococcus aureus (13%) and Streptococcus spp. (15%).
- Secondary: necrotizing pancreatitis, small bowel strangulation, and viscus perforation. Gram-positive organisms are more prevalent with upper GI pathology than gram-negative organisms are with lower GI pathology, depending on the origin of the peritonitis. E. coli, Klebsiella, Proteus, Streptococcus, Enterococcus, Bacteroides, and Clostridium are prevalent species; Staphylococcus epidermidis and S. aureus are the most frequent causes of PD peritonitis.
RISK ELEMENTS
Advanced cirrhosis with ascites, malnutrition, upper GI hemorrhage, use of PPIs, and past SBP are all indicators of SBP.
- Acid suppression, which is most frequently achieved with PPIs, encourages gut bacterial translocation and growth.
- Patients with Child-Pugh class C cirrhosis account for 70% of SBP cases.
- Risk is increased by low ascites protein (1.0 g/dL).
Secondary: intestinal perforation brought on by IBD, trauma, or Helicobacter pylori, NSAID- or Helicobacter pylori-induced ulcers, vascular disease-induced intestinal ischemia, alcohol abuse-induced pancreatitis,
PD peritonitis: - Nonsterile method - New equipment
DURATIONAL PREVENTION
SBP prophylaxis reduces mortality in patients at high risk (such as those with esophageal varices, ascites fluid protein concentrations below 1.0 g/dL, or a history of SBP).
Norfloxacin, ciprofloxacin, TMP/SMZ PO, and ceftriaxone IV are examples of antibiotics.
SBP prophylaxis should also be given to cirrhotic ascites patients who have low ascitic fluid protein (1.5 g/dL), renal impairment (creatinine 1.2 mg/dL, BUN 25 mg/dL, serum sodium [Na] 130 mEq/L), or liver failure (Child-Pugh grade 9 and blood bilirubin 3 mg/dL).
Limit your PPI usage.
Sterile methods and antibiotic prophylaxis before specific treatments are recommended for PD peritonitis.
CONDITIONS OFTEN Associated with
SBP nearly invariably happens when cirrhosis is decompensated.
DISEASE HISTORY
SBP: cirrhosis and/or ascites history, fever, chills, changes in mental status, diffuse, persistent abdominal discomfort that may be hardly noticeable because of the existence of ascites, nausea/vomiting, diarrhea, and GI bleeding
Secondary: Unless a history of perforation, abscess, or other intraabdominal pathology or recent surgical intervention is present, it may be clinically indistinguishable from SBP Tertiary: Persistent symptoms despite initial treatment or a history of recurrent peritonitis Presumptive diagnosis of PD peritonitis in PD patients with cloudy effluent
ALERT
30% of people may not have any symptoms.
PHYSICAL EXAMINATION: Tachycardia, tachypnea, altered mental status, hypotension, hyperthermia, or hypothermia — AMS may be subtly manifest; the Reitan trail test (connect-the-numbers test) is useful for spotting subtly manifested changes in mental status. If the patient requires more time to complete the test than is typical for their age, consider the possibility of hepatic encephalopathy.
There is no stiffness because ascites divides the parietal layer of the peritoneum from the visceral layer, causing abdominal discomfort and distention, ascites, abdominal wall guarding, rebound tenderness, hypoactive/absent bowel sounds, and diarrhea.
DIFFERENTIAL DIAGNOSIS Hepatitis and decompensated cirrhosis are liver diseases. Luminal diseases include abscess formation, ileus, volvulus, intussusception, mesenteric adenitis, pancreatitis, cholecystitis, malignancy, peritoneal carcinomatosis, and inflammatory bowel disease (IBD). Extraluminal diseases include ruptured ectopic pre
Rapid evaluation and early diagnosis lower mortality.
Initial examinations (lab, imaging)
 CBC: anemia and leukocytosis
- SBP is predicted by thrombocytopenia 100,000/mL (1)[B].
BMP: azotemia and metabolic acidosis
Cirrhotics frequently have aberrant LFTs and coagulations at baseline, and SBP is almost always detected by cirrhotic ascites and CRP >60 mg/L (1)[B].
• Secondary:
- An abscess, perforation, or other infection source may be visible on abdominal x-rays or CT scans.
Procalcitonin levels can be used to indicate severity; a level of >10 ng/mL is associated with ICU admission.
Tests in the Future & Special Considerations
Prior to administering antibiotics, get cultures from the ascites, blood, and urine.
If the patient is asymptomatic and the culture is monomicrobial but the PMN is 250, colonization typically disappears, but if the patient is symptomatic, colonization typically advances to SBP.
If the culture is polymicrobial but the PMN is less than 250, traumatic paracentesis was probably the etiology.
 Broad-spectrum antibiotics are necessary if the culture is negative but the PMN is greater than 250.
SBP and alcoholic hepatitis can happen simultaneously.
In cases of hemorrhagic ascites, the PMN count is adjusted by deducting 1 PMN for every 250 RBCs.
Other/Diagnostic Procedures
Culture, Gram stain, cell count with differential, albumin, and for secondary peritonitis, LDH, total protein, glucose, alkaline phosphatase (ALP), and CEA are ascitic fluid tests from diagnostic paracentesis.
SBP: The greatest individual predictor of SBP is PMN >500 cells/mm3 (86% sensitive; 98% specific). A threshold of 250 cells/mm3 has a 94% specificity and 93% sensitivity.
- The diagnosis of SBP is supported by PMN > 250 cells/mm3, a positive ascitic culture, and the absence of a secondary peritonitis-causing factor.
- A serum-ascites albumin gradient of less than 1.1 g/dL eliminates portal hypertension and excludes out SBP.
PMN >250 cells/mm3 on ascitic fluid analysis with polymicrobial culture and/or two of the following (Runyon criteria) are indicators of secondary peritonitis. LDH > upper limit of normal for serum, glucose 50 mg/dL, and ascitic fluid total protein >1 g/dL (67% sensitive, 96% specific)
ALP >240 U/L or CEA >5 ng/mL are indicators that perforation is likely (sensitivity 92%, specificity 88%).
- A pancreatic source is indicated by an ascites-to-serum amylase ratio >6.
Peritonitis due to PD: Positive effluent culture, consistent clinical symptoms, and peritoneal fluid are two of the possible diagnoses. WBC > 100 mm3 with > 50% PMN

Management 
Salt restriction, spironolactone, furosemide, albumin infusion following large-volume paracentesis, and/or lactulose for encephalopathy are all ways to control ascites.
Stop using -blockers in SBP.
Avoid using drugs that are nephrotoxic.

Medication 

Without recent use of a -lactam antibiotic, community-acquired SBP should be treated with third-generation cephalosporins, ideally cefotaxime 2 g IV every eight hours for five more days.
- SBP: ofloxacin 400 mg BID PO (must be renally dosed) can replace cefotaxime in the absence of prior quinolone use/prophylaxis, vomiting, shock, hepatic encephalopathy, or serum creatinine >3 mg/dL (2).[A]
Cefotaxime 2 g IV q8h while awaiting sensitivity for symptomatic bacterascites with PMN count 250 cells/mm3.
- Fluoroquinolones (levofloxacin), piperacillin/tazobactam, or vancomycin are examples of second-line antibiotics.
Patients for whom cephalosporins are contraindicated or poorly tolerated can utilize ciprofloxacin 200 mg IV BID.
Adding 1.5 g/kg of albumin within six hours and 1 g/kg on day three is advised for SBP patients with renal or hepatic impairment (serum creatinine >1 mg/dL, BUN >30 mg/dL, or total bilirubin >4 mg/dL).
The majority of individuals benefit from a 5-day parenteral antibiotic regimen.
- Patients with the following infections may require longer treatment:
Reevaluate the patient after a 5-day treatment of antibiotics if there are any unusual or resistant organisms (like Pseudomonas).
- If asymptomatic, no more therapy is required.
- Repeat the paracentesis if the fever or pain lasts.
• Secondary:
- IV cefotaxime or another third- to fourth-generation cephalosporin along with metronidazole, empiric broad-spectrum antibiotic coverage for polymicrobial illness
A third level:
- If there are no leaks or perforations that have not been healed, keep up with medical management: broad-spectrum antibiotics (directed by susceptibilities), early enteral feeding, and prevent atrophy.
- You might want to apply antifungal protection.
- If PD-related infection is persistent or recurrent, think about removing the catheter.
Peritonitis due to PD
Unless the patient is septic, IP rather than IV administration of antibiotics is preferred.
- Vancomycin or a first-generation cephalosporin (such as cefazolin) for gram-positive coverage
- Gram-negative coverage: a carbapenem, an aminoglycoside, or a third-generation cephalosporin (such as ceftazidime, cefpime)
- The majority of patients typically get better 48 hours after starting antibiotic therapy.
Clinical improvement, a less hazy efferent, and/or a decrease in the number of cells in the peritoneal fluid are all signs that the infection is going away.
PD does not need to be stopped.
Remove catheter if you have: - Mycobacterial or fungal peritonitis - Peritonitis with high WBC in peritoneal fluid and culture-negative peritonitis with persistent symptoms
After a 5-day treatment of antibiotics (for refractory peritonitis), the PD effluent is not clear.
 Four weeks after finishing an antibiotic regimen, peritonitis returns.
Laparotomy is necessary; if the catheter is taken out, it can be reinstalled if the symptoms have subsided after two weeks.

Procedures and Surgery 

Medical care solely for SBP (80% mortality if patient with SBP has exploratory laparotomy) Secondary: First-line surgical management includes source control with open laparotomy to repair any perforated viscus and remove infected material.
Tertiary: Additional surgery for serious abdominal infection is associated with worsening and mortality even if there are no unrepaired holes or leaks.

Caution 
If surgical treatment is not provided, the fatality rate of subsequent bacterial peritonitis approaches 100%.

Admission 

Hospitalization is usually necessary for acute peritonitis.
Use invasive monitoring in conjunction with goal-directed fluid treatment in patients with cardiogenic or septic shock.
Peritonitis patients may arrive extremely hypovolemic, therefore volume resuscitation is essential.
Patients with cirrhosis frequently take -blockers. A-blockers prolong hospital stays, increase mortality, and worsen hepatorenal syndrome during an episode of SBP.



Patient Follow-Up Monitoring
Improvement can be seen when vital signs return to normal and leukocytosis disappears.
After 48 hours, a repeat paracentesis is recommended, but it is not necessary if there has been a clinical improvement because a PMN decrease of more than 25% is anticipated.
Especially in cases of secondary peritonitis, total parental nutrition (TPN) and NPO are recommended for diet.
Resuming enteral feeding after bowel movement has returned can help prevent ascites in the future.

SBP prognosis: For inpatients with a first episode of SBP, mortality is 5% when diagnosed and treated right away.
- If antibiotics are started early, before shock or renal failure set in, the prognosis improves.
- Renal insufficiency is the most powerful predictor of poor prognosis.
Patients with past SBP have a 40–70% 1-year recurrence rate and a 50–70% 1-year death rate.
Secondary: 20% of treated patients die in hospitals.
- The prognosis for perforation peritonitis is worse than for nonperforation peritonitis, and the death rate for perforation approaches 100% if surgical treatment is not received.
 2-6% death rate from PD peritonitis (fungal, gram-negative, and S. aureus infections are the most common)
- A 5-20% HD switch

Abdominal compartment syndrome, fistula formation, secondary infection, iatrogenic infection, renal and hepatic failure, encephalopathy, and coagulopathy are among the complications.
 Respiratory failure, ARDS, adrenal insufficiency, cardiovascular collapse, and sepsis/septic shock

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