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Diagnosis Deconstructed

Diagnosis Deconstructed: Natural Selection After Eight

Morchi, Ravi MD

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doi: 10.1097/01.EEM.0000440688.21270.e0

    It was before 8 p.m. when he arrived at an open-air area where a medical assistant wrote basic admission orders. No intervention can be initiated under the stars, however.

    On the ward. My colleague and I note abdominal pain of recent onset. No distension. No incarcerated hernia. Deep palpation affords a wince, but no involuntary reflexive guarding by rectus or oblique muscles.

    IV fluids are started per the order “two liters Ringer's lactate at moderate rate.” Here crystalloids are in bottles not bags, and there are only three rates: slow, moderate, and fast. He is given one dose of pethidine IV and paracetamol PR. IV antibiotics directed at typhoid and other enteric organisms are initiated.

    The decision seemed simple. He did not need anything else at this hour. Mobilizing more resources is difficult, and it would be impossible in a few minutes. I decided natural forces would keep him safe for the night.

    After 8 p.m. in this hospital, not much happens. No monitors light up the darkness, no alarms populate the quiet of the night, there's very few nursing staff. All patients lie together in the same room, either comfortable or in pain, for the next 12 hours. The families of each patient loyally sit on the floor next to their loved one. Staff sleep on two chairs strategically placed facing each other. No one will contact you for any event transpiring overnight. After 8 p.m. in this hospital and others like it around the globe, you have to relegate your patient to natural selection.

    At 7 a.m., medicine opens its doors again. In daylight, antibiotic doses will be given, bottles of Ringer's changed, pain assessed and treated, and vital signs recorded every six hours. It is at this time that I come to his bedside for morning rounds.

    Is this he? He looks so different. I am not sure I recognize him. This man looks little like the one I admitted last night. He looks ... horrible.

    Apparently natural forces had not been kind to him. Respirations were cut shallow and rapid. I look down at a taut, distended abdomen with drum-like consistency and guarding diffusely. His entire abdominal wall assumes rigidity upon a slight tap of my index finger. He would not move. He barely wanted to breathe. I would not have predicted that this man, out of so many, would be the one to require more.

    The alternative. I suppose it is better than what I have woken to many past mornings.

    Conducting rounds, the morning nurses follow along from bed to bed until I get to one in particular. Where is he? Discussion ensues about a man admitted last night who is now nowhere to be found. Not in the cot where he lay just 12 hours ago. His family is also gone. What happened to him? Where did he go? Invariably, the first person I ask has no idea. So the nurses convene and in one dialect or another find someone, possibly a family member of an adjacent patient, who can enlighten us on the situation. Then one spokesperson surfaces to address my question in English.

    “He has passed.” In the middle of the night generally. Routinely described “gasping” and then “passing” by a single observer. The body is immediately moved to a back shed. Family disperse for the night.

    Diagnosis? I often have no idea. No autopsy. No further questions. Death is accepted here. This alternative is not uncommon. I have inquired about the missing man, woman, or child many times. It has been happening for years. Somewhere in a rural district hospital of a low-income country, it is happening right now.

    Our man. The next move is clear. Conservative care was not a friend to him. Fortunately, he is not yet a statistic. Not yet a memory tucked in a shed. I contact our anesthetist, and he prepares the operating theater. Foley catheter and NG tube are placed. I inform my emergency medicine colleague that she will be assisting me. She also wonders what has gotten hold of our man.

    Perforated duodenal or gastric ulcer. Having traveled back in time to the pre-PPI era, it is the most common, rapidly progressive abdominal sepsis that is the culprit here. Thin patients with unimpeded erosion of their proximal gut mucosa will perforate, and have little omentum to wall off the process. Diffuse peritonitis ensues. I prepare mentally for an upper abdominal incision, closure of my imagined duodenal perforation, and tacking an omental patch. As we prep, I ask my customary question to our nurse anesthetist.

    “Justice, what do you think it is? Perforated ulcer?” For all my training and thousands of dollars' worth of education in an advanced modern-day medical system, my guess at the diagnosis is generally not as accurate as his. Justice is a native. Treating his own people for decades with little more than a nursing degree, he can sense the illness brewing under the skin. He is familiar with its smell.

    “No,” he says, looking down as he pushes the ketamine. “I think it is dead bowel.” Uh oh.

    Carefully through the linea, I find the color shining from under the peritoneal lining is black. No whoosh of air upon opening. Instead loops of distended black bowel crawls out of the incision and rise toward the sky. I extend down to his symphysis and up to his xiphoid.

    The cause? The majority of jejunum and ileum twisted. I feel for his cecum, and it is in the correct place. I note the root of his small bowel mesentery under his transverse mesocolon. He has midgut volvulus without malrotation.

    I look up at the hospital's only monitor and see a fast heart rate but normal BP. Why is he not in distributive shock? Why did he not become the alternative statistic last night? The same reason an initial lactate or ABG would be unimpressive. Fortunately, this deception is not a factor in a place without labs.

    Obstructed venous return. Venous return is blocked first in closed loop obstruction. Venous congestion is followed by arterial insufficiency as tissue pressure rises above capillary pressure. But lactate and other ischemic metabolites generated cannot escape this sequestered circuit. They are trapped, imprisoned in this portion of the portal circulation behind a twisted, knotted superior mesenteric vein and so not visible on labs drawn from an antecubital vein or the radial artery.

    Purple bowel would have been more promising. Detorsing it, feeling for pulsation in its mesentery, and watching it under a warm lap pad, purple bowel can be viable. Soon to turn pink. But black bowel, that is different.

    Not wanting to see the systemic, acidemic, distributive shock that volvulus had spared him hours ago, I choose not to detorse him. Averting a rush of prisoners through the SMV that will overwhelm liver sinusoid defenses, flood hepatic veins, stream through right and left heart, and pour into systemic arterioles. Resultant vasodilation will mean a drop in blood pressure, loss of perfusion to every vital organ, and then cardiac arrest.

    Instead I ligate mesenteric vessels and resect. One man minus seven feet of dead intestine is still alive. Hand-sewn, end-to-end anastomosis of jejunum to remaining ileum. We extubate him and move him back to the monitorless, alarmless wards to fend for himself after 8 p.m. Night by night.

    Impressively he lives. We care for him to the best of our resources, and every morning he is still there. Not yet a statistic. I begin to wonder about nutrition, fat absorption, and vitamin B12. In a few days he is discharged to face the long-term challenges of malabsorption in sub-Saharan Africa.

    The phrase “pain out of proportion to exam” pertains only to early ischemia confined to the inner mucosal lining of bowel. Without involving the serosa yet, indentation of the parietal peritoneum down against such serosa does not produce reflexive contraction of abdominal wall muscles. The patient writhes in pain from ischemic mucosa, but his exam is not impressive.

    In time, ischemia extends outward to include intestinal muscle and serosa, too. Now your patient has pain in proportion to exam. Guarding and rigidity to percussion. Light taps are enough to indent the peritoneal lining against black bowel: direct evidence of events transpired in a sequestered circulation behind an obstructed mesenteric vein, in spite of potentially unimpressive indirect measurements taken from the antecubital vein or radial artery.

    Natural forces? They were not so bad after all. Mesenteric venous occlusion spared his life that first night.

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