Signout. The off-going team knew he was ill, but I want to start with the story as I saw it. His temperature had risen from 36.2° to 39.4°, and his heart rate was up to 140 beats per minute by my evaluation. Blood pressure remained at 110s/60s. Respirations would reach as high as 30. He was not hypoxemic. A mildly uncomfortable 50-year-old man who was unaware of his own past medical history.
Effortless tachypnea with no deficiency in oxygenation and no work of breathing? The driving force behind his respirations is not within the pulmonary parenchyma. Probably blowing off a metabolic acidosis.
Hours earlier my colleagues had found the source. A small lower back abscess, just superior to the gluteal cleft. Spontaneously draining. The patient claimed it had been there for almost a week. An infected pilonidal cyst.
Other than this, he was unimpressive to my eye. Awake and alert with no skin or mucous membrane findings. No embolic or immunologic phenomenon suggestive of a tattered, infected valve.
By auscultation also unremarkable. Lungs were clear with no prolongation to expiration or wheeze and no rales on inspiration. Heart was regular without systolic or appreciable diastolic murmur. Normal S1 and S2 and no extra heart sounds.
But by touch he had problems. PMI was bounding. Vigorous LV contractions punching against the chest wall. His fingers and toes were warm, and extremity pulses had a rapid upstroke and downfall. Even when the summation of contractility, preload, and arteriolar tone work together to manufacture the façade of normotension on the monitor, touch tells me he is vasodilated and his heart is frantic.
And touch would tell me more. He was tender, edematous, and firm above and below the spine of the scapula on the right. These findings extended to the posterior, proximal upper arm. Passive range of motion was only minimally painful to rotation and abduction of the shoulder. Active range of motion, however, was very limited.
And then there was his calf. Tender and edematous and limited in active ankle plantar flexion. Two sites? Time to ask the soft tissue question, and start our descent.
Begin at the dermis. He had no significant erythema or palpable inflammatory process. One layer deeper: I do not expect inflammation confined to the SQ to limit active range of motion.
Fascia? Whispers of “nec fasc” circulate among oncoming and off-going teams. This is certainly a possibility, but I sometimes feel the term encourages us to jump to conclusions without considering the intervening and surrounding anatomic layers.
In my experience, by the time the feared monomicrobial variant of necrotizing fasciitis sets into multiple limbs, patients are generally very impressive to sight and not just to touch. Their mental status is altered and their attempts at compensating with arteriolar tone fail. Their blood pressure dips. Their lactate rises.
I scroll through his labs. Lactate of 2.4 on initial draw. A repeat is pending. With multiple limbs and an unimpressive inspection, I am not sold on the rapid advancement of Streptococcus pyogenes. It can remain on the differential, but it is not first in line. Could it be a slower, less aggressive polymicrobial necrotizing process? Sure, but better to set aside this catch-phrase for now and keep moving.
Muscle. Limitation to active range with relatively preserved passive motion brings us here. His tenderness seems localized to discrete muscle groups. CK is normal. Muscle need not be necrosed when an entity like this erupts. Just a little further to be sure.
Joint. It normally remains a sequestered environment in the absence of trauma or surgery. I imagine the synovial lining, cartilaginous bony coverings, and ligamentous boundaries at his glenohumeral area all working normally. His passive range of motion is too good for acute septic arthritis that is simultaneously producing systemic changes. Vitals out of proportion to range of motion move me away from the joint.
Bone. No pain with axial loading of the humerus into the glenoid or along the talus-tibia-femur bone line. Palpating cortex through tender soft tissue is difficult, but the axial load technique allows us to detour and assess bone integrity indirectly. Pain with axial load while the patient's finger points to a site far removed from your hands? I believe the patient has a bony problem right there. With normal load, he could still have osteomyelitis decompressed into adjacent soft tissue, but first we must address what is clearly involved.
Pyomyositis. Not necrosing muscle. Rather lakes of pus amid inflamed, infected myofibers whose integrity is otherwise maintained. Intact fascia contains the entire process and so the superficial SQ and skin are often normal. It is generally hematogenous in origin. He must be bacteremic and seeding multiple sites. The source? It brews under the covers. Better make sure it is adequately decompressed.
Source control. An important component of goal-directed therapy. He receives crystalloid, vancomycin, Zosyn, and clindamycin, and under local anesthetic, we find a few dozen more milliliters of pus percolating in an infected pilonidal vault.
CT scan of his chest and shoulder showed enlarged muscle groups at the supraspinatus, infraspinatus, teres minor, and posterior and lateral deltoid on the right. Consistent with the exam. Both CT and touch have brought us to muscle. One of the very few worthy recipients of a pan-man-scan. His lower extremity showed tensor fascia latae thickening plus right vastus lateralis and left gastrocnemius muscle asymmetry.
The surgical consult called by the off-going team was not motivated to take the patient on their service. With a lactate trending down, improving vitals, and a normal mental status, I was satisfied with antibiotics for the immediate future. His bicarbonate had dropped from 20 to 16 with IV fluid resuscitation, but I believed this was still consistent with his improving clinical picture. Having treated the contraction alkalosis of volume depletion, we unmask the real extent of an underlying ketotic anion gap medical acidosis. No worse than before, just better visualized. Our patient is admitted to the medical ICU, waiting to cross paths with our surgical consultants once again.
Five days later he is in the OR having purulence drained from five separate muscle compartments. His blood cultures, pilonidal abscess, and urine in the meantime all grew MRSA. Inpatient teams learned he had a history of a pyogenic liver abscess populated by Streptococcus viridans requiring IR-guided drainage in the distant past.
What is the problem with infantry? His single-file marching, single-shot, musket-bearing neutrophils are normal in number, but must not be normal in function. Qualitative defects to chemotaxis, migration, or phagocytosis? I think back to medical school and haunting catch-phrases of chronic granulomatous disease and inherited leukocyte adhesion, myeloperoxidase, and granule deficiencies. Reviewing his inpatient labs a week later, I find the answer to a history of fatigued granulocytes may be much simpler: a hemoglobin A1C of 13.
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