A 1-year-old fell off the back of a truck just outside the hospital. Her airway and breathing are intact. Systolic blood pressure is 80, pulse is 150, her extremities feel cool, and capillary refill is prolonged.
Circulation. We should not be satisfied with the aggregate number when looking at blood pressure. How fast does the heart have to beat to generate the aggregate number? How much of the BP is created by constricted arterioles starving their distal capillary beds? The composite of 80 in this case does not equate with adequate perfusion.
Lacking a universal donor blood, a saline bolus is started. Type and crossmatch are sent. We use whole blood; no component therapy here. The family is asked to donate before transfusion can begin, and medical volunteers often give blood in emergencies.
Her pelvis is stable, her abdomen slightly distended. No guarding, but enough to clue us in. Blood does not aggravate the parietal peritoneum much, but gastric contents, pancreatic juice, feces, and urine bound for the outside are irritating to the peritoneal lining. Blood, on the other hand, is endogenous. Mesodermal in origin, it produces the least impressive abdominal exam.
Blind four-quadrant needle aspiration has been replaced by ultrasound. Her FAST is positive in the upper quadrants. Pericardial space is negative.
Brain. Pediatric GCS: E2V3M5. A coordinated response to pinching fingers, toes, upper arms, and thighs; sensory input is processed by association areas, motor cortex, basal ganglia, and cerebellum. The result descends the CNS as a meaningful response by moving a limb away from stimulus. M5 tells us that a lot of neurons in multiple parts of the brain are working together. This is the most important point in the coma scale. M4 and M3 suggest a spinal cord liberated from damaged or compressed cerebral cortices above, which may require empiric cranial exploration for extra-axial blood and decompression.
Cord. She is moving all extremities. We stabilize her cervical spine. Secondary survey: No major facial injuries, limb threats, perineal trauma; urine is clear.
Her response is not good despite whole blood. Heart rate continues to rise to the 160s despite resuscitation. Extremities remain cool and capillary beds white. We cannot tolerate a dip in mean arterial pressure if she has a head injury. She is teetering on it: strained myocardium and starved distal vascular beds are scrounging to produce a respectable MAP for vital organs. Component deconstruction of the BP tells me her persistence at 80 is a failure: She is still bleeding.
Our anesthetist is not keen on operating tonight. Most hemoperitoneum he sees is a subacute or chronically ruptured ectopic pregnancy where we have hours to act. We can auto-transfuse in the OR by ladling hemoperitoneum through a gauze sieve into a metal bowl and then back into a previously prepped blood bag. Crude but effective if the blood isn't contaminated by bowel contents. Patients have SIRS post-operatively but generally fare well.
Eight o'clock is approaching. Most staff will go home, and our girl will be left to live or die. No monitors or alarms, and we do not have one-on-one care. It's now or not at all.
Theater. Our anesthetist agrees, and prepares her with ketamine and diazepam. No general anesthesia here, no intubation or mechanical ventilation. Midline incision from xyphoid to pubic symphysis down to linea. I see dark blood. Not knowing if there is concomitant bowel injury contaminating hemoperitoneum, we cannot commit to auto-transfusion. I use suction to remove 600 mls of blood from the peritoneal cavity. A significant percentage of her circulating volume sits in the suction canister.
Exploring quadrant by quadrant, I find the source: a fractured spleen with a laceration extending into the hilar vessels that is still bleeding.
Textbooks say these injuries are often managed non-operatively in children, that the capsule is stronger than in adults. Children may have better hemostatic capacity within their splenic vessels and sinusoids. Chronic daily battles with malarial parasitemia and hematogenous bacterial transit leave spleens here three times the size of those at home. Our patient does not appear to conform to what American texts say.
Incising the splenorenal ligament posteriorly allows for mobility in reflecting the spleen medially and exposing vasculature. Clamps are placed across short gastric vessels. I clamp, dividing and doubly ligating the major vessels, and remove her spleen to inspect: no further bleeding. She has ectopic splenic tissue near her pancreatic tail. Maybe this will grow and spare her from future malarial catastrophe? Or I could slice a few pieces of spleen and embed them under the peritoneal reflection laterally, hoping vasculature will grow into splenic autografts.
She has an uneventful recovery. Mentation improves as she receives more blood. We discuss vaccination, prophylactic antibiotics, and antimalarial measures. Capillary beds pink up, extremities are warm, and her heart rate comes down to 100. We measure systolic pressure one more time: 80. Success.
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