3. National lead for GlobalSurg Collaborative
National Lead with GlobalSurg® for FALCON trial
Co-Prinicipal Investigator for NRPU grant
Collaborator for European Coloproctology society, UK
Colorectal Fellowship, Yonsei University, South Korea
Fellow of College of Physicians & Surgeons, Pakistan
(Surgery)
Fellow of Higher education authority of UK (FHEA)
Member of Royal College of Surgeons, England (UK)
Member of College of Physicians & Surgeons, Pakistan
(Surgery)
Member Editorial Board, BMJ case reports since 2011-2014
Reviewer for Rawalpindi Medical Journal since 2015
Dr. Ahmad Uzair Qureshi
4. Management of Peritonitis
General Care
Correction of fluid and electrolyte
imbalance
Broad-spectrum antibiotic
therapy
Insertion of nasogastric drainage
tube and urinary catheter
Vital system support
Surgical Principle
Remove or divert cause
Peritoneal lavage ± drainage
Analgesia
18. Familial Mediterranean fever
(periodic peritonitis)
• Mutations in the MEFV (Mediterranean fever) gene
• Abdominal pain and tenderness, mild pyrexia, polymorphonuclear
leukocytosis
• Role of Surgery
19. Tuberculous Peritonitis
• Mycobacterium avium- (HIV) co-infection.
• The abdomen is involved in 11% of patients with extrapulmonary TB
• Ileocaecal is the most common site of involvement)
• Ascitic fluid is typically a straw-coloured exudate
• Protein >25–30 g/L
• White cells >500 mm3
• Lymphocytes >40%.
20. Tuberculous Peritonitis
• Acute (may be clinically indistinguishable from acute bacterial
peritonitis) and chronic forms
• Abdominal pain, sweats, malaise and weight loss are frequent
• Ascites common, may be loculated
• Caseating peritoneal nodules are common
• Intestinal obstruction may respond to anti-tuberculous treatment
without surgery
Editor's Notes
usually include local symptoms and/or signs of peritonitis, GI upset (secondary to ileus, e.g. nausea and vomiting), signs of systemic inflammation (hyper- or hypothermia, chills, tachycardia and tachypnoea ± signs of septic shock), worsening liver and renal function, hepatic encephalopathy and GI bleeding. It should, however, be noted that evolving infection may be asymptomatic, especially in outpatients.
The diagnosis is made by paracentesis, and this should be considered in patients with cirrhosis and ascites even when there is a low index of suspicion. Some guidelines recommend diagnostic paracentesis in all patients with cirrhosis and ascites on hospital admission. The diagnosis is made by an increased neutrophil of 250/mm3 as determined by counting centrifuged ascitic fluid. Ascites culture is negative in as many as 60% of patients with clinical manifestations of SBP
and increased ascitic neutrophil count. When culture is positive (40% of cases), the most common pathogens include gram-negative bacteria, usually E. coli, and gram-positive cocci (mainly streptococci and enterococci).
The diagnosis is made by paracentesis, and this should be considered in patients with cirrhosis and ascites even when there is a low index of suspicion. Some guidelines recommend diagnostic paracentesis in all patients with cirrhosis and ascites on hospital admission. The diagnosis is made by an increased neutrophil of 250/mm3 as determined by counting centrifuged ascitic fluid. Ascites culture is negative in as many as 60% of patients with clinical manifestations of SBP
and increased ascitic neutrophil count. When culture is positive (40% of cases), the most common pathogens include gram-negative bacteria, usually E. coli, and gram-positive cocci (mainly streptococci and enterococci).
The diagnosis is made by paracentesis, and this should be considered in patients with cirrhosis and ascites even when there is a low index of suspicion. Some guidelines recommend diagnostic paracentesis in all patients with cirrhosis and ascites on hospital admission. The diagnosis is made by an increased neutrophil of 250/mm3 as determined by counting centrifuged ascitic fluid. Ascites culture is negative in as many as 60% of patients with clinical manifestations of SBP
and increased ascitic neutrophil count. When culture is positive (40% of cases), the most common pathogens include gram-negative bacteria, usually E. coli, and gram-positive cocci (mainly streptococci and enterococci).
usually include local symptoms and/or signs of peritonitis, GI upset (secondary to ileus, e.g. nausea and vomiting), signs of systemic inflammation (hyper- or hypothermia, chills, tachycardia and tachypnoea ± signs of septic shock), worsening liver and renal function, hepatic encephalopathy and GI bleeding. It should, however, be noted that evolving infection may be asymptomatic, especially in outpatients.
Primary pneumococcal peritonitis
This may complicate nephrotic syndrome or cirrhosis in children. Otherwise healthy children, particularly girls aged between 3 and 9 years, may also be affected, and it is likely that the route of infection is sometimes via the vagina and fallopian tubes. At other times, and always in boys, the infection s blood borne and secondary to respiratory tract or middle- ear disease. The prevalence of pneumococcal peritonitis has declined greatly and the condition is now rare. In brief, the clinical onset is sudden, with pain usually localised to the lower half of the abdomen. The temperature is raised to 39°C or more and there is usually frequent vomiting. After 24–48 hours, profuse diarrhoea is characteristic. There is usually increased frequency of micturition. The last two symptoms are caused by severe pelvic peritonitis. On examination, peritonism is usually diffuse but less prominent than in most cases of a perforated viscus, leading to peritonitis. A leukocytosis of ≥30 000/μL, with approximately 90% polymorphs, suggests pneumococcal peritonitis rather than another cause, e.g. appendicitis. After starting antibiotic therapy and correcting dehydration and electrolyte imbalance, early surgery is required unless spontaneous infection of pre-existing ascites is strongly suspected, in which case a diagnostic peritoneal tap is useful. Laparotomy or laparoscopy may be used. Should the exudate be odourless and sticky, the diagnosis of pneumococcal peritonitis is practically certain, but it is essential to perform a careful exploration to exclude other pathology. Assuming that no other cause for the peritonitis is discovered, some of the exudate is aspirated and sent to the laboratory for icroscopy, culture and sensitivity tests.Thorough peritoneal lavage is carried out and the incision closed. Antibiotics and fluid replacement therapy are continued and recovery is usual. Other organisms are now known to cause some cases of
primary peritonitis in children, including Haemophilus spp., group A streptococci and a few gram-negative bacteria. Underlying pathology (including an intravaginal foreign body in girls) must always be excluded before primary peritonitis
can be diagnosed with certainty. Idiopathic streptococcal and staphylococcal peritonitis can also occur in adults.
Familial Mediterranean fever (periodic peritonitis) is characterized by abdominal pain and tenderness, mild pyrexia, polymorphonuclear leukocytosis and, occasionally, pain in the thorax and joints. The duration of an attack is 24–72 hours, when it is followed by complete remission, but exacerbations recur at regular intervals. Most of the patients have undergone appendicectomy in childhood. This disease, often familial, is limited principally to Arab, Armenian and Jewish
populations; other races are occasionally affected. Mutations in the MEFV (Mediterranean fever) gene appear to cause the disease. This gene produces a protein called pyrin, which is expressed mostly in neutrophils; however, the exact function
of pyrin is not known. Usually, children are affected but it is not rare for the disease to make its first appearance in early adult life, with cases in women outnumbering those in men by two to one. Exceptionally, the disease becomes manifest in patients aged >40 years. At surgery, which may be necessary to exclude other causes (but should be avoided if possible), the peritoneum is inflamed, particularly in the vicinity of the spleen and the gall bladder. There is no evidence that the interior of these organs is abnormal. Colchicine therapy is used during attacks and to prevent recurrent attacks.