1996, Flagstaff, Arizona. An 18-year-old man presents to a local clinic with left groin pain. He has had fever and diarrhea for two days. He reports having fallen prior to the onset of symptoms. He is afebrile but tachycardic to 120. Physical exam notes left groin swelling and tenderness. He is diagnosed with a muscle strain and given NSAIDs.
The next day paramedics arrive at his house because he has collapsed in the shower. Cardiopulmonary arrest ensues. He is transported to the emergency department and pronounced dead.
“Groin strain.” What exactly did they see in that clinic? What did they feel in his inguinal region and medial thigh that generated this diagnosis? A simple strain of the adductor compartment muscle? Misdiagnosed adductor compartment myonecrosis? Or something else?
That same year, western Colorado. A 16-year-old girl presents to the local ED with pain and numbness in her left arm. She has subjective fever, chills, and multiple episodes of vomiting. She reports having fallen from a trampoline five days earlier. Tachycardic to 100 but otherwise afebrile and not tachypneic. After a physical exam and chest x-ray, the patient is diagnosed with a brachial plexus injury and given neurology follow-up.
Two days later, she is found obtunded at home and brought back to the ED. Febrile to 102.5°F, tachypneic to 50, and tachycardic to 170, she deteriorates and suffers a respiratory arrest in the department. A pulse returns with intubation and resuscitation, and the patient is transferred to the nearest tertiary care center, only to die later that day.
Septic shock and severe metabolic acidosis. Vasodilation and decreased contractility from acidosis drop brainstem perfusion and thereby stifle her respiratory drive. Inadequate CO2 exhalation compounds her metabolic acidosis, and her pH spirals down. The result is worsening vasodilation and plummeting cardiac function causing her to arrest. The respiratory component is reversed with intubation, and the pH rises high enough to regain meaningful myocardial motion and vascular tone. The underlying acidosis and systemic inflammatory response march on, however, and eventually consume her.
Was her brachial plexus injury related? Could motor deficits be attributed to neural dysfunction? Or was strength testing and muscular function actually limited by pain? Just what did they see along the course of the plexus in the supraclavicular area and axilla that drew their eyes and minds to crisscrossing axons and fascicles?
2009, Qinghai Provence, China. A herdsman finds his ailing dog lying in distress 6 km from home. The hound had hemoptysis and hematemesis, and the herdsman carried him over his shoulders to be buried. Four days later, the herdsman developed a fever and cough, and was brought to a local clinic by relatives. Doctors described him as having a pale complexion and bloody sputum. They initiated IV ceftriaxone and recommended he go by private vehicle to the Tibetan Hospital in Xinghai County.
The patient began to vomit violently on the way to the county facility with his brothers. He died later that day. His brothers and father-in-law would transport his body back to be prepared and buried in traditional Tibetan fetal position. The father-in-law, who likely had a prominent role in the preparation of the body, would fall ill with respiratory complaints and expire days afterwards.
The herdsman also had met briefly with a friend from his village before departing, and that friend would soon develop hemoptysis and die. Nine other close contacts would develop symptoms, but survive after timely antibiotic treatment.
Abrupt onset of fever and hemoptysis followed by a rapid clinical decline? Sounds like a necrotizing pulmonary process. Transmitted by close contact during expectoration of bloody sputum, it is the pneumonic variant of our other deadly dealings in Colorado and Arizona. But no groin strains or plexus injuries here.
Although rare, the pulmonary route of transmission was described in outbreaks in Oakland, Los Angeles, and Manchuria in the early 1900s. Today we fear its potential as a biologic weapon. The other modes of inoculation are more common. The bite of an infected flea from a rodent, prairie dog, or even a pet is one way to start the process. Exposure to secretion or exudate from a dead or dying animal is another. Shortly thereafter a tender enlarged lymph node emerges. This is not just reactivity to antigen by component macrophages and lymphocytes in “adenopathy.” It is actually an intra-nodal war properly termed “adenitis.” If not examined carefully, this conglomerate of active macrophages, T cells, and B cells dueling directly with the invading organism can be missed. It is exquisitely tender, and may limit range of motion or send “shooting” pain down a limb.
Lying just centimeters from the brachial plexus or adductor muscle compartment, “neuropathy” and “muscle strain” are anchors in the cursory exam of an unwary clinician who chooses not to probe deeply into flexural surfaces with his fingertips.
Prominent gastrointestinal symptoms and systemic illness coming out of an endemic area are the only clues in cases without a tender node.
It has consumed millions upon millions of preindustrial human lives. And today it still manages a handful in high-activity regions. If unrecognized and untreated at its bubonic stage, it may progress to a secondary pneumonic form. What follows then is the steep descent of a necrotizing respiratory process similar to the fate of a Tibetan herdsman carrying his lovable and loyal dealer of death across his shoulders.
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