ABDOMINAL INFECTIONS AND PUERPURAL SEPSIS Samuel Mwaniki OBJECTIVES

ABDOMINAL INFECTIONS AND PUERPURAL SEPSIS Samuel Mwaniki

OBJECTIVES �Describe pathogenesis & clinical characteristics of intra-abdominal infections �Identify most likely etiologic organism(s) �Review appropriate drug therapy

INTRA-ABDOMINAL INFECTIONS Infections contained within the peritoneum or retroperitoneal space. Peritoneal cavity contains: � Stomach � Jejunum, Ileum � Appendix � Large intestine (colon) � Liver, gallbladder and spleen Retroperitoneal space: � Duodenum � Pancreas � Kidneys

Intra-abdominal Infections �Appendicitis �Peritonitis �Intra-abdominal Abscess �Diverticulitis �Antibiotic-Associated Diarrhea - Clostridium difficile �Food Poisoning/Traveler’s Diarrhea – E. Coli �PUD - Helicobacter pylori �Pelvic Inflammatory Disease

GI Microflora Stomach: �H. Pylori, Lactobacilli Upper Intestine: �Streptococci, Enterococci, Staphylococci, E. Coli, Klebsiella, Bacteroides Ileum: �Streptococci, Staphylococci, Escherichia coli, Klebsiella, Enterobacter, Bacteroides, Clostridium Colon: �Bacteroides, Peptostreptococci, Clostridium, Bifidobacterium, Escherichia coli, Klebsiella, Enterobacter, Enterococci, Staphylococci

Peritonitis Inflammation of the serous lining of the peritoneal cavity due to: �Microorganisms �Chemicals �Irradiation �Foreign body injury

Primary (Spontaneous Bacterial Peritonitis) �No focus of disease is evident �Arises without a breach in the peritoneal cavity or GIT �Bacteria transported from blood stream to peritoneal cavity (Cirrhosis, CAPD) �Usually monomicrobial

Secondary �Acute perforation of the GI tract (diverticulitis - ), appendix (appendicitis), gallbladder, tumor perforations) �Community acquired or nosocomial �Usually polymicrobial �Post-operative peritonitis �Post-traumatic peritonitis

Tertiary �Peritonitis in a critically ill patient which persists or recurs at least 48 h after apparently adequate management of primary or secondary peritonitis

Clinical Symptoms � Abdominal pain �Anorexia (N/V) �Fever (38 -40 ºC) �Abdominal distention and tenderness �Hypoactive or faint bowl sounds �Leukocytosis

Normally: � 20 to 50 m. L transudate �Peritoneal membrane measures approx. 1. 7 metres square �WBC < 300 cells/mm 3 �Protein: <3 g/d. L Bacterial peritonitis: � 300 to 500 m. L inflow/hr resulting in hypovolemia. �WBC > 300 cells/mm 3 �Gram stain + for bacteria

Microbiology �Blood cultures often –ve �Peritoneal fluid used (parecentesis) �Health care associated intra-abdominal infection usually due to nosocomial organisms particular to the site of the operation and specific hospital and unit

�Community acquired infections �infections derived from stomach, duodenum, biliary system and proximal small bowel: � Gram positive and Gram negative aerobic and facultative bacteria �distal small bowel: � Gram negative facultative and aerobic bacteria � Anaerobes �large bowel: � Facultative and obligate anaerobic bacteria � Streptococi and enterococci commonly present

Aerobes: �GN Bacilli: E. Coli, Klebsiella, Enterobacter, Proteus mirabilis, Pseudomonas aeruginosa �GP Cocci: Enterococcus spp e. g. E. faecalis, Streptococcus, S. aureus, Coagulase –ve Staphylococcus

Anaerobes: �GN Bacilli : B. fragilis, Prevotella, Pophyromonas �GP Cocci: Clostridium spp, Peptostreptococcus. Fungi: �C. albicans

Appendicitis � Highest incidence 10 -19 y/o � Male > female � Pathophysiology: Relationship to onset of sx 0 -24 h after sx onset: obstruction within appendix , inflammation & occlusion of vascular & lymphatic flow, bacterial overgrowth then necrosis. >48 h after sx onset: perforation, abscess/peritonitis Early sx: dull, non-localized pain, indigestion, bowel irregularity, flatulence Later sx: pain/tenderness more localized, N/V, Fever > 39 degrees celcius, leukocytes >15000: perforation likely

Management Acute, non-perforated appendicitis � cefazolin + metronidazole Perforated appendicitis �Cover enteric gram – rods and anaerobes (2 nd/3 rd generation ceph or FQ) + metronidazole, Cefoxitin, piperacillin/tazobactam, ampicillin/sulbactam, imipenem �Antibiotics are started before surgery, continued for 7 - 10 days �Switch to PO based on patient status

Intra – abdominal Abscess �Abscess: purulent collection of fluid, necrotic debris, bacteria, inflammatory cells that is walled off/encapsulated by adjacent healthy cells in an attempt to keep pus from infecting neighboring structures. �Encapsulation can prevent immune cells/abx from attacking contained bacteria, low O 2 in capsule, anaerobes thrive here! � A Result of chronic inflammation, develop over days-yrs �Located within peritoneal cavity or visceral organs �May range from a few milliliters to a liter in volume

Ruptured abscess �Spread of bacteria + toxins into peritoneum - peritonitis �Spread of bacteria + toxins into systemic circulation – sepsis, multi-organ failure, death Presentation: �Nonspecific low grade or spiking fever, abdominal pain/discomfort +/- distension Labs: �Leukocytosis, +/- positive blood cultures, +/hyperglycemia �Ultrasound, GI contrast study, or CT scan may be used for evaluation

Microbiology �Usually mixed infection: aerobes & anaerobes within the same abscess �E. coli �Klebsiella �Enterococci �B. fragilis �Clostridium

Management Combination of modalities: �Surgical: Prompt drainage of abscess (secondary peritonitis) and/or debridement, Resection of perforated colon, small intestine, ulcers, Repair of trauma. �Support of Vital functions: Blood pressure/fluid replacement, Monitor heart rate, Monitor urine out put (0. 5 ml/kg/hr) �Appropriate antimicrobial therapy

Empiric Antibiotic Therapy MUST include aerobic/anaerobic coverage Agents with Aerobic and Anaerobic activity: �Ampicillin/sulbactam - (enterococci) �Piperacillin/tazobactam - (enterococci) �Imipenem/cilistatin � Meropenem �Ertapenem �Aminoglycoside + clindamycin or metronidazole �Tigecycline �Moxifloxacin - (active against 83% of Bacteroides strains) + metronidazole

Antibiotic Associated Diarrhoea �Antibiotic therapy (broad spectrum agents: clindamycin, ampicillin, 3 rd generation cephalosporins are most common) �Disruption of normal colonic flora �C. difficile colonization (gram +, spore forming anaerobe) �Release of toxins A (enterotoxin), B (cytotoxin), & binary toxin �CDT (associated w/ recent outbreaks) �Damage to colonic mucosa (pseudomembranous plaques), inflammation, intestinal fluid secretion

Treatment FIRST LINE: �Metronidazole (Treatment of Choice) � 250 mg PO QID or 500 mg PO/IV TID x 10 -14 days ALTERNATIVE: (if pregnant, not responding to metronidazole or recurrences) �Vancomycin � 125 mg PO QID x 10 -14 days +/- rifampin 600 mg PO BID Always stop the drug responsible for causing the infection as soon as possible!

PUERPURAL SEPSIS Definition of Puerpurum 1. The time from the delivery of the placenta through the first few weeks after the delivery. 2. 6 weeks in duration. 3. By 6 weeks after delivery, most of the changes of pregnancy, labor, and delivery have resolved and the body has reverted to the non pregnant state.

Puerperal Infection Any bacterial infection of the genital tract after delivery. Incidence: 6%. The most important cause of maternal death. Puerperal Morbidity Temperature 38. 0℃ or higher, the temperature to occur on any 2 of the first 10 days postpartum, exclusive of the first 24 hours, and to be taken by mouth by a standard technique at least four times daily.

Risk factors 1. Anaemia 2. Hemorrhage 3. Episiotomy and CS 4. Placenta retention 5. Hospital contamination

Common pathogens 1. Aerobes � Group A, B, and D streptococci � Gram-negative bacteria: Escherichia coli, Klebsiella � Staphylococcus aureus

2. � � � Anaerobes Peptostreptococcus species Bacteroides fragilis group Clostridium species 3. Other � Chlamydia trachomatis � Mycoplasma species

Manifestation � Acute vulvitis, vaginitis, cervicitis and endometritis � Uterine infection � Adnexal infections � Septic pelvic thrombophlebitis � Sapremia (blood poisoning resulting from absorption of putrefaction matter from the uterus)

MERCI BEACOUP, MADAME MADEMOISELLE ET MESSRS!