Acute Abdomen – Sepsis – CIRCI: A Success Story

K. Lakshmanan, Inbarasu, Vinoth Selvin, APS. Kannan, Yogesh

Department of Anasethesiology, Kauvery Hospital, Tirunelveli, India.


Evaluation of acute abdomen is difficult because various factors can obscure the presentation delaying or preventing the correct diagnosis, with subsequent adverse patient outcome. Multiple diagnoses must be considered which pose a diagnostic challenge but timely intervention is necessary to limit morbidity and mortality.

Case Presentation

A 38-year-aged male came with complaints of abdominal pain nausea, vomiting for 5 days and admitted in a private hospital, treated as Diabetic Keto Acidosis (DKA) since his blood sugar was high and urine was positive for acetone, and referred to our hospital in view of breathlessness for one day.

On admission, he had normal sensorium with GCS of 15/15 with respiratory rate of 35/min, pulse rate of 135/min, BP 130/80, Temperature 101°F, RBS 325 mg/dl. He was well built and seemed to be severely dehydrated. Examination revealed diffuse abdominal tenderness, abdominal distention with sluggish bowel sounds. Acute Abdomen with perforation or obstruction was suspected.


There was leucocytosis, elevated sepsis markers and elevated Renal parameters. ABG showed severe metabolic acidosis. He had high blood sugars and was positive for urine acetone. USG abdomen report suggested ileus.


On Day 2 he had hemodynamic instability with worsening metabolic acidosis (pH 6.9); hence intubated and ventilated. Ryle’s tube aspiration showed faeculent matter. CVP was placed in Right Internal Jugular Vein (IJV), with hourly CVP monitoring. CT Abdomen showed distal small bowel obstruction. Patient was planned for emergency laparotomy by Surgical Gastro Enterologist.

Intra operatively distal ileal stricture with gangrene of small bowel were found and planned for resection and anastomosis. Intra operative periods were uneventful.

On Day 3, patient’s condition was worsening, with Acute Kidney Injury (AKI) and electrolyte abnormalities. The patient was requiring high dose vasopressors with mild improvement in acidosis. Critical illness-related corticosteroid insufficiency (CIRCI) was suspected and patient treated with steroids and Thiamine.

On Day 4, after 12 h of initiating steroids, patient had a remarkable improvement in hemodynamics and acidosis was corrected. His HR: 90/min, BP: 150/90.

On Day 5 patient was extubated in view of good hemodynamic stability and GCS. Patient was in a phase of resolving AKI.

On Day 7 abdomen was soft, bowel sounds were present, patient passed stools and flatus. Patient initiated on oral fluids and normal diet thereafter.

On Day 10 antibiotics was de-escalated and discharged on Day 12.


Acute abdomen presents a symptom complex with suggests a disease that probably threatens life and demands and urgent diagnosis for early treatment. When the obstruction lies in the jejunum or high in the ileum the colic appears in waves at interval of 3-5 min. This interval becomes longer in obstruction of the terminal ileum where it is about 8-10 min. The site of pain will give an indication as to the site of obstruction. Vomiting is a fairly constant symptom. Upper small bowel obstruction vomiting is much more frequent than obstruction in the terminal part of the small bowel. It takes about 3 or 4 days in complete intestinal obstruction for the vomitus to become faeculant. Distention may not be very early sign. For constipation to present as a significant sign one has to wait for another 24 h. The higher the obstruction more will be dehydration due to tremendous loss of water and electrolytes.

Sepsis is a life-threatening condition that arises from a dysregulated host response to infection. The invading microorganism and its proteins are pathogen associated molecular patterns (PAMP) that are recognized by the host’s intracellular and extra cellular pattern recognition receptors (PRR), which leads to the activation of various pro inflammatory and anti-inflammatory pathways.

Thiamine pyrophosphate is a coenzyme of glyoxylate which oxidizes glyoxylate to carbon dioxide. Thiamine is thus believed to protect against the side effect of renal oxalate stone formation by vitamin C. Thiamine is also cofactor in the production of neuro transmitters and has antioxidant properties. There may be a subset of patients who may benefit from targeted metabolic resuscitation.

Critically ill patients are at their physiological extremes, and are in a ‘stress response’.

CIRCI – critical illness related corticosteroid insufficiency- is characterized by inadequate intracellular glucocorticoid-mediated anti-inflammatory activity for the severity of the patient’s critical illness, which results in dysregulated systemic inflammation. Random plasma cortisol level below 15 mcg/dl has been defined as a cut off for diagnosing adrenal sufficiency. A random free cortisol level of 1.8 mg/dl should be considered as cut of value to diagnose patient at risk for adrenal insufficiency.

Acute kidney injury has been categorized into three main forms, (1) Pre renal (2) Intrinsic (3) Postrenal. Generally, urine sodium less than 20 mmol/L along with The Fractional Excretion of Sodium ( FENa) less than 1% implying 99% of filtered sodium is reabsorbed supporting prerenal form. UNa > 40 mmol/L along with FENa > 1% favour intrinsic form. Serum sodium concentration does not affect FENa making it more sensitive than UNa in diagnosing pre-renal AKI. In patients on diuretics FEUrea has emerged as a potential substitute based on the concept that diuretics affect reabsorption of urea to lesser extent as compared to sodium. Similarly, near biomarkers KIM-1, NGAL, IL-18 have proved to be better predictors than FENa regarding progression of AKI in critically ill patient. Fractional excretion of potassium (FEK) has also been studied as a marker of AKI. Values between 10% and 15% are considered indicative of pre-renal AKI.

Traditionally The Acute Kidney Injury Network (AKIN) and the Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease (RIFLE) classification were used for identification and classification of AKI. To overcome short comings these two criteria were combined. Kidney Disease Improving Global Outcomes (KDIGO) proposed a new definition for AKI in the year 2012. According to the KDIGO, AKI is defined as any of the following:

(1) Increase in serum creatinine by 0.3 mg/dl within 48 h.

(2) Increase in serum creatinine to 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days.

(3) Urine volume <0.5 mL/kg/h for 6 h.

Acute kidney injury is classified into three stages based on the severity of the disease.


Acute abdomen and sepsis are common in clinical practice and should be considered whenever clinical features and investigations points towards the diagnosis. Prompt diagnosis, selective and appropriate imaging studies and timely surgical intervention yield satisfactory results


We would like to thank our colleague in the Department of Anaesthesiology, Kauvery hospital Tirunelveli, for contribution towards the treatment of this patient.


Dr. K. Lakshmanan



Dr. Inbarasu



Dr. Vinoth Selvin



Dr. APS. Kannan



Dr. Yogesh