Two men carry an exhausted young woman through the hospital doors, her arms draped over the backs of their necks, her thighs supported in the air by their hands. I take it that they are her family. No gurney, no wheelchair. Her head flops back as she stares at the ceiling.
Her abdomen appears large. “Another obstructed labor,” I think to myself. The heaviest of burdens carried by women in this particular land. Cephalopelvic disproportion and pushing for more than a day, rupture of membranes hours ago now with chorioamnionitis, a boggy distressed uterus with a thinned-out lower segment that is nearly ruptured, and a future vesicovaginal fistula from ischemic breakdown of the urethra and posterior bladder wall as it is smashed between the pubic symphisis anteriorly and the fetal head posteriorly.
At least, that is how it usually plays out. At C-section I expect to find all of this and a fetus that is limp and often dies. The surgery is to save mom and the five other children who already rely on her. To add a sixth living child is a bonus.
I step up to her cot, and as I place my hand on her abdomen, the thoughts on my lips are to summon the anesthetist. He is a nurse by training, with an extra year or two of education using spinal analgesics and ketamine. I will need his help to get this done.
But she is not gravid. It is not the uterus. On bimanual exam, her cervix is not dilated or effaced.
Instead she has ridges across her taught abdominal wall, ridges that mark the edges of tubular-shaped bulges, tubes with diameters anywhere from four to six centimeters. They writhe, and she writhes with them. Episodic pain and distorted facial grimaces mirroring the movement of the ridges. This is the colic of small bowel peristalsis against a fixed obstruction.
She needs IV fluid. Liters of volume are already lost into her small bowel lumen, soon to transudate into her peritoneal cavity. As the intestine distends, pressure in the wall of the small bowel approaches capillary pressure. Perfusion is then compromised and ischemic changes follow. Ischemia starts on the inner submucosal lining and percolates outward through the wall and toward the serosa.
A nasogastric tube can decompress her stomach and maybe even a bit of her proximal duodenum as the pylorus opens, but the majority of jejunum and ileum will fail to decompress with this tube. Intraluminal and intramural pressures will rise in this distal small bowel, and ischemia will ensue.
How will we know? She will develop the cardinal sign that a luminal process has progressed through the full thickness of the bowel wall and now involves the outer serosa.
Involuntary Guarding. When you press down on the abdomen, if the parietal peritoneum touches ischemic or inflamed bowel serosa, then a spinal reflex takes hold and results in contraction of the rectus and oblique muscles, muscles meant to protect the underlying peritoneal lining from coming in contact with sick serosa.
It is reproducible in depth and location with each focused palpation because the serosa sits at a set distance below. Linked to the speed of neural connections, timing of the contraction is identical with each dip of the parietal peritoneum. These characteristics make it involuntary.
She has the finding not only to palpation but also to light finger percussion. The next step up will be a rigid abdomen and curtailed inspiration.
Small bowel obstruction. The most common causes in the western world are adhesions from surgery, closed loop obstruction in a hernia, and colonic processes like neoplasm ensnaring a loop of small bowel.
But here, where I am at this moment, colon cancer is rarely found at laparotomy. My patient has no hernia on exam. Prior TB peritonitis or PID could be the source of adhesions, I suppose, but her abdomen bears no scars of past surgeries. The cause of her bowel obstruction, I would soon discover, could have been treated simply at a much earlier stage. A stage capped by symptoms of dyspepsia and crampy abdominal pain … and sometimes, a particular cell on CBC.
Eosinophils. I found myself not liking eosinophils in medical school. Other immune cells seemed to do all the work. Eosinophils meanwhile would be caught in the drama of a hypersensitivity response or allergic reaction; overreacting to something or other, and making the patient suffer as a result of this cell's generalized anxiety disorder and panic attacks.
Why do we even have them? What do they offer to the good fight? As I prepare to explore this woman's abdomen, I take a moment to reflect.
Neutrophils are infantry. They valiantly go to battle and attempt to eat invading organisms. Phagocytosis. Macrophages like to eat, too, but they can also join hands under the instruction of the commanding generals we call T-lymphocytes, walling off larger invaders and those that resist being eaten: incarcerating the prisoners of war in a granuloma.
But what if the organism is too large to be eaten and too powerful to be incarcerated? Who do we call on when the organism is not a single cell but composed of multiple cells? Multiple cells linked together and squirming through the skin, liver, or intestines of our patients? Who can battle the giant, inedible multicellular dragons of the infectious world? Not the neutrophil or macrophage but their comrades-in-arms that contain within them powerful explosives. Upon degranulation, the explosives can keep at bay even the largest of invaders. Explosives that stain red with acid dyes, giving the eosinophil its name.
Laparotomy. I run the intestine from the ligament of Treitz toward the terminal ileum, and notice that the bowel appears more dusky and congested distally, the serosa showing the signs of elevated intraluminal and intramural pressures compromising capillary perfusion. The source of obstruction is near.
I can feel the distal ileal loops filled with entangled, spaghetti-like structures that want to burst through the intestinal walls. The peak of this knotted mess of pasta lies just proximal to the ileocecal valve, a narrow juncture and the most common point for a foreign body to lodge.
I place a purse-string suture, and open the terminal ileum to find dozens of spaghetti staring back at me. I use ring forceps to shepherd them toward the enterotomy and pull them out of the terminal ileum. Hundreds of strands of pasta later, the obstructing bolus is cleared and ileal patency re-established.
One of the most common causes of small bowel obstruction in children in sub-Saharan Africa, Ascaris has been known to cause the occasional blockage in an adult. It is unnoticed early on because a few luminally localized multicellular pathogens produce only crampy pain and a soft abdominal exam with lack of serosal involvement. At that point, it is up to a wary clinician, anti-helminth tablets, and the bravest granulocytes we have to keep it from becoming an emergency.
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Dr. Morchiis the director of the Medical Screening Examination program at Harbor UCLA Medical Center and an assistant professor of emergency medicine at UCLA's David Geffen School of Medicine.
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