Case description

An infant born at 23 weeks (birth weight 670 g) after preterm prolonged rupture of membranes and chorioamnionitis had a course typical of extreme prematurity: intubation and surfactant on the first day, extubation on day 4 to non-invasive support, caffeine, phototherapy, early hyponatremia with acute kidney injury, and feeding intolerance managed with continuous feeds. By 29 weeks corrected (weight ~1 kg) the infant was on bubble CPAP +7 in 25–30% oxygen and tolerating fortified expressed breast milk by gavage, with the central line already removed.

During a care, the nurse noted feeding intolerance and abdominal distension. Within an hour the abdomen had become markedly distended and then rigid, oxygen requirement rose, and the infant became poorly perfused with weak pulses. The chest radiograph showed very low lung volumes with severely dilated, thick-walled bowel loops and no free air. A capillary gas showed pH 6.83, pCO₂ 97, bicarbonate 15 and a lactate of 10, rising on repeat to 13.7 with a potassium of 8. The infant was intubated, but ventilation remained very difficult despite high pressures and a trial of high-frequency oscillation, with pre-ductal saturations in the 70s.

A cardiac POCUS was performed at the bedside at this point, while the team was securing access. Views were difficult because of the tense abdomen and no subcostal window could be obtained. The study showed an “empty heart”: both ventricles were severely underfilled with near-obliteration of the cavities in systole (“kissing ventricles”), the atria were small, and there was no patent ductus arteriosus. Despite this, biventricular contractility was preserved (LV fractional shortening 38% on M-mode, TAPSE 0.65 cm) and there was no pericardial effusion, no tamponade physiology and no outflow tract obstruction. Left ventricular output was low, with an LVOT velocity-time integral of only 4.3 cm (Vmax 0.46 m/s); the RVOT VTI was 8.3 cm (Vmax 0.70 m/s). The constellation an empty hyperdynamic heart and an inability to ventilate, in an infant with a rigid abdomen, anuria and loss of lower-limb pulses, pointed to acute abdominal compartment syndrome as the cause of the collapse: intra-abdominal hypertension compressing the IVC and renal veins, limiting venous return to the right atrium, and splinting the diaphragm so that lung volumes and venous return fell further with every increase in ventilator pressure.

 Vascular access was extremely difficult; once a peripheral line was obtained, normal saline boluses (10 mL/kg, repeated) were given and broad-spectrum antibiotics started. Blood pressure fell to 53/24 (28) mmHg, lower-limb pulses could no longer be palpated and no post-ductal saturation could be obtained. On examination the abdomen was tense and rigid, with reducible right inguinal and umbilical hernias. There was improvement of the filling of the 4 cavities after administration of 20 mL/kg of NS. 

General surgery was called urgently. After multidisciplinary discussion at the bedside, including the parents, the consensus was that bedside decompressive laparotomy and exploration was the only option that could restore venous return. As soon as the abdomen was opened and decompressed, heart rate and saturations normalised immediately, confirming the obstructive-restrictive physiology. 

Cardiac POCUS teaching points

1. Acute abdominal compartment syndrome is a preload problem first. Intra-abdominal hypertension compresses the IVC and hepatic and renal veins, so venous return to the right atrium falls abruptly. The right ventricle has nothing to pump, pulmonary blood flow falls, and the left ventricle is in turn underfilled. The heart is small, hyperdynamic and “kissing”, exactly as seen here, and the IVC is collapsed rather than distended. This is the opposite of tamponade or RV failure, where the IVC is plethoric.

2. The lungs are part of the same compartment. Cephalad displacement of the diaphragm reduces lung volumes and compliance; the ventilator pressures needed to oxygenate further raise intrathoracic pressure and further impede venous return. Hypercapnia, hypoxemia and shock are therefore linked, and escalating ventilation can worsen the hemodynamics.

3. Fluid is a temporising measure, not a treatment. Boluses transiently raise the mean systemic filling pressure and may briefly improve filling, but as long as the abdomen is tense, venous return remains obstructed. Decompression is the definitive therapy; the immediate normalisation of heart rate and saturations on opening the abdomen illustrates this.

4. Cardiac POCUS is useful for what it excludes as much as for what it shows. In a collapsing infant, the bedside study ruled out tamponade, myocardial dysfunction, outflow obstruction and a hemodynamically significant ductus within minutes, and the empty, hyperdynamic heart with a collapsed IVC redirected the team toward the abdomen rather than toward more inotropes.

5. Preserved contractility is not reassuring in this setting. A normal fractional shortening and TAPSE with a very low LVOT VTI mean the ventricle is contracting well on an inadequate volume; output is limited by filling, not by the myocardium.

6. Loss of lower-limb pulses and anuria are signs of the same process, reflecting both the low cardiac output and direct compression of the abdominal aorta, its branches and the renal veins.

Cardiac POCUS views

Cardiac POCUS after 20 mL/kg of Normal Saline

References 

• Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013;39(7):1190–1206.

• Carlotti AP, Carvalho WB. Abdominal compartment syndrome: a review. Pediatr Crit Care Med. 2009;10(1):115–120.

• Thabet FC, Ejike JC. Intra-abdominal hypertension and abdominal compartment syndrome in pediatrics. A review. J Crit Care. 2017;41:275–282.