He has been here for two weeks now being treated for cellulitis and a DVT. They say he is definitely improving. Just not normal yet.
“How did you get heparin?” I ask.
Apparently, they had a small supply in pharmacy. That's new; probably a random donation. It will not last long. He was diffusely swollen and not entirely improving on flucloxacillin, so subcutaneous heparin was added three days earlier.
“Can he walk?”
It is odd to see a patient who cannot ambulate because of inflammation in the subcutaneous plane alone. DVT may impair mobility, I suppose, but his gait seems intensely painful with each step. This is not typical of either diagnosis.
Something is missing in the approach. I ask the visiting medical student who is managing him. She endorses that he has gotten much better with treatment. But still, he lies here with a swollen lower leg and an inability to walk.
OK, I guess I'll round on him again tomorrow. Maybe he will show continued improvement.
Tomorrow comes and so does the day after, and he seems to have plateaued. He is eating, has no fevers or tachycardia, and has transitioned to PO antibiotics. He is comfortable at rest. I attempt to ambulate him and again the exquisite pain. As he hops around, his knee remains in 30 degrees of flexion. I lay him back in bed.
Exam. Toenails, pads of digits, and soles are covered in a thick rind of black dirt. This is normal here. He has a number of small, healed ulcerations on his feet and the anterior surface of both tibia, also not unusual. Any one of them could have gone on to become a tropical ulcer. I note a small hump of non-tender dorsal pedal edema. This can be seen in venous congestion, lymphatic insufficiency, or inflammatory capillary leak. Nonspecific.
Encompassing his lower leg in my hands and comparing it with the other side, his calf is measurably larger and warmer. He has mild induration posteriorly and proximally in the calf. This finding persists as I walk up the lower leg to the popliteal fossa and distal posterior thigh.
Our main question in evaluating the soft tissue should be one of depth. Just how deep do we need to go to get an answer?
Epidermis. Generally painless with a palpable border or scale, epidermal inflammation is mostly fungal, superficial bacterial (impetigo), or an irritant or allergic phenomenon. Patients may itch, but pain is not common because these receptors are not present in the epidermis.
Dermis. He has evidence of ulcerations dipping into this layer, but they are old and scarred. No active process. Tenderness and induration are seen, yet the classic discrete palpable border of dermal pathology like furuncles, carbuncles, and erysipelas is not present. Instead, our patient's induration fades into and out of adjacent normal tissue. And I cannot attribute his trouble with ambulation to discomfort from the stretch of the dermis. So we must search deeper.
Subcutaneous tissue. This is where our student has settled, and in fact, where most of us settle. Cellulitis is inflammation at the subcutaneous level, with some secondary dermal changes from cutaneous vasodilation. The faded borders to induration favor the diagnosis. But limitations to bearing weight and extension at the knee are atypical.
Fascia. What occupies our minds most often in the United States is a monomicrobial necrotizing process rapidly devouring fascial planes longitudinally up and down a limb or trunk. This process may not percolate to the surface until late in the game, involving the dermis as blotchy ecchymoses or hemorrhagic bullae only after hours or days. All we are presented with early on is invisible, indurated, exquisitely tender fascia and a systemic inflammatory response.
But I notice that such a rapidly advancing process is uncommon here. If it exists, most patients will succumb in their village or hut. Transit times to the hospital are on the order of days; if these patients are out there, they generally remain out there.
If this were his story, he must be the rare survivor of the acute phase, and now is in some odd, subacute balance with the microorganism, the features of which we would not see often in the modern medical world because of earlier presentations, advanced imaging, targeted antibiotics, and prompt surgical intervention.
Rather than the march of Streptococcus, what we see in the developing world is a slowly percolating, polymicrobial type of anaerobic necrosis that smolders on for days. Necrosis, yes, but at a pace that allows for presentation to the hospital, diagnosis, and debridement multiple times over the course of weeks.
Like with fasciitis, he is very tender and lacks dermal findings to explain his tenderness. But he doesn't smell like anaerobic necrosis. And his pain and induration are focal: just a circumscribed locale to his proximal calf and the distal posterior thigh. Time to descend.
Muscle. Tibialis anterior and peroneus muscles are soft and nontender. I passively stretch these compartments via ankle plantar flexion and inversion, and note no twinge of discomfort.
Gastrocnemius and soleus. This is the superficial posterior compartment, and it is here that he is most tender and indurated. He jumps consistently with only a finger prod into his proximal gastrocnemius. Very focal. Too focal for fasciitis, in my opinion. Is this a myositis? Passive stretch to the superficial posterior compartment by ankle dorsiflexion produces no pain. That is odd. I would expect him to jump at ankle motion. Similarly he has no problem with stretch of the deep posterior compartment as I extend all his toes.
And proximally? His induration rides along the biceps femoris tendon and the tendons of the semimembranosus and semitendinosus. It seems to represent taut musculotendinous units that have remained contracted over the past few weeks in response to the lower leg process, rather than direct extension of that process. An impending contracture that does not permit complete extension of his knee; it is a secondary, not primary, issue.
Vasculature. Just underneath and between muscle compartments, we find ourselves in the deep venous system. This is the second place that clinicians settle reflexively. Ignoring the intervening tissue, cellulitis and DVT seem to be our fallback diagnoses.
Portable ultrasound. The most practical and useful imaging modality of the resource-poor setting, ultrasound's value exceeds x-rays and rudimentary lab tests. I visualize and compress his CFV, SFV, and PV. No DVT, as far as I can tell. But what of the soft tissue? As predicted, no cobblestoning for cellulitis. No sheets of fluid floating over fascial planes. Instead, enlarged, disarrayed muscle fibers of the superficial posterior compartment, in comparison with normal fiber alignment in the other leg. I think we have found our problem.
Bone. I obtain an x-ray to exclude any obvious involucrum or sequestrum of osteomyelitis that could have secondarily decompressed into muscle over the past few weeks. It is negative. And then it is off to make the diagnosis.
Accessing all four compartments for fasciotomy can be accomplished from two lengthwise incisions on the lateral and medial sides of the lower leg. I am looking only at the superficial posterior compartment, so I start with a medial longitudinal incision and cut down to fascia. Dermis and SQ are edematous but not remarkable. I note the fascia is intact and strong. Nothing breaks under blunt finger pressure. Upon incising the fascia, it comes pouring out … pus.
Pyomyositis is a tropical condition where hematogenous seeding by Staphylococcusaureus produces purulent lakes that can fill any muscle compartment. Occult locales like the iliopsoas generally go unrecognized early on or are misdiagnosed as septic hip. The problem is most common in the thigh and lower legs, however, and typically has no necrosis or ischemia. Presentations are subacute or chronic, and pain with passive stretch and other signs of compartment syndrome may not be present. After fasciotomy and decompression, I take him back daily for repeat blunt exploration and dressing changes until the compartment dries up. He is eventually discharged ambulating again.