A diabetic middle-aged man presents with four days of fever, mild headache, and upper back and neck pain. He endorses nasal congestion and a hoarse voice. On exam, he appears comfortable with a heart rate of 100 and temperature of 39°C.
Viral URI? He has symptoms but no signs. Compression of each nasal passage reveals he can breathe freely through an unobstructed, opposite nare. No nasal discharge for rhinitis, no palatal or pharyngeal erythema for pharyngitis, and no actual hoarseness to his voice suggesting laryngitis. His epiglottis is hidden just out of view, but at this point I cannot call it a URI.
Skin, lung, urine? We look next at interfaces with the environment. No erythema or induration over the extremities. Normal breath sounds and rate. No cough or prolonged expiration. Chest x-ray is negative. No symptoms of cystitis or prostatic enlargement, his suprapubic area and CVA are not tender, and a urinalysis sent earlier is normal.
Abdomen? Start the cavity search. He is neither elderly nor immunocompromised, so I can rely on a key finding. Indenting his peritoneal lining, I feel for reflexive abdominal muscle contraction indicating contact with an inflamed structure below.
No guarding in the left upper quadrant or lower abdomen to suggest inflamed gastric or bowel serosa. No response high in his epigastrum, just under his xiphoid, in the area of the esophagogastric junction. Just north of his umbilicus, the abdominal wall overlying his pancreas remains soft.
Cupping my fingers under the right costal margin, he has no reaction over the gallbladder fundus or with deeper palpation just medially over the area of the common bile duct. Wrapped in fat and tucked snugly between the duodenum inferiorly and the liver superiorly, the common bile duct does not abut the peritoneum when inflamed. I cannot rule out cholangitis by palpation alone. I look at his eyes: no icterus.
LP? The cavity search continues, but now we ask if infection resides in a sanctuary more difficult to assess at bedside because it is protected by bone and without a direct interface to the outside world. Shining a light close in either eye, he does not wince. Guiding his neck down in flexion, he claims mild discomfort at the base. Is this meningeal irritation or myalgia of the trapezius muscle? Shoulder shrug and palpation of the muscle do not reproduce the discomfort. Lumbar puncture shows a normal opening pressure, normal protein, and no white cell elevation.
Fever without a clear source. Possible viral syndrome. Well appearing. Discharge from ED? Not yet. A standard approach to fever may yield nothing, but a better investigation is waiting to be done.
Skin again. No erythema. But just what surfaces did we visualize? The inner upper arm? Proximal thigh? The underside of abdominal skin folds? The perineum of a diabetic? We should look more closely at these places when reflexology ends and something just doesn't seem right
Below the dermis, the subcutaneous fat can range from a centimeter or two in thickness to more than a foot in depth. We call an inflammatory process residing here cellulitis. Dermal changes are secondary.
Deep to the subcutaneous lie fascia and muscle. Inflammation at this level need not be visible at the skin surface. If we do not see anything superficial, do we feel anything deeper? Exquisite tenderness unexplained by any overlying skin changes? Necrotizing fasciitis and myositis have begun in this way: focal pain and one abnormal vital sign.
Mucous membranes revisited. Although the pharynx appears normal, crevices in the forefront of the oral cavity need exploration. Were his upper and lower lips everted to inspect the labial-gingival mucosal folds? Decaying dentition, exposed pulp, or loose teeth indicative of periodontal disease? Any could serve as portals for clinically significant bacteremia.
On the other end, his anal and rectal mucosa provide daily defense against millions of microorganisms. Any evidence that they have been breached?
Parapharyngeal space. The anterior parapharyngeal space does not escape clinical detection often. The area I am interested in is actually posterior to the ramus of the mandible, where phlegmon or abscess is not visible and does not engage the masseter or the medial pterygoid to cause trismus. Patients may have a "sore throat," "hoarse voice," or other upper respiratory symptoms, but mucous membranes will appear normal. They may not create stiffness to neck motion as in a retropharyngeal process. The closest I can get to the secluded posterior parapharyngeal space is to wrap my fingers behind the ramus and see if he reacts to pressure in this area.
Epidural space. The diagnosis is often not made on the first visit. Inflammation here is outside the thecal sac, and so CSF may not sample it. Anything on midline or paramidline percussion of the spinal column? Infection can arise from neighboring intervertebral discs, bone, or venous plexus.
Cardiovascular. The last cavity to consider when fever appears and cannot be localized. The pericardial lining produces pain when inflamed, so we can move past that and look at the myocardium. A normal cardiovascular exam cannot rule out myocarditis, but without symptoms or signs of heart failure, this diagnosis should remain a distant possibility rather than a probability. What interests me more is what we see after we open the heart and look inside.
Endocardium. The inner lining of the chambers is continuous with valve leaflets. Sometimes only a soft diastolic rumble on cardiac exam and not always accompanied by a known risk factor, subacute bacterial endocarditis can be a difficult diagnosis. The major Duke criteria needed for a definitive diagnosis are not often met in the ED. Leave the center of the body to search for corroboration.
Extremities. Are there signs of embolic or immunologic phenomenon? The distal areas come to our aid, accumulating intravascular debris lodged in small vessels. The same can be said for conjunctiva and retinal vasculature. These findings can be seen in up to half of cases, provided we look.
Spleen tip. Unless pathologically enlarged, it is not represented in the left upper quadrant exam. You have to move it into view by shifting the patient to his right side to find it, pushing at the posterior axillary line and feeling for the tip anteriorly with your other hand. The spleen can be enlarged when it is asked to clear the plasma of infectious matter.
Renal. No bacteria in his urine, but is the sediment consistent with inflammatory debris sprinkled onto glomeruli?
Follow the endocardium out of the left ventricle and past the aortic valve leaflets. The lining is now vascular endothelium. Infections particular to the endothelium include Rickettsia species.
Detach from the endothelium, and survey the blood. Just what is in there? Gram positives, gram negatives, spirochetes, viruses, and occasionally fungi or helminths can all populate the plasma component. Gram stain is normal, and blood cultures brew in the lab. Screening HIV serology is negative.
So far nothing secures the diagnosis of subacute bacterial endocarditis or identifies a pathogen within the plasma component. Just one more place to go.
The cellular component of blood. His white blood cell count and hemoglobin were normal, and his platelet count was 93. Some infections are known to make their living inside immune cells; Salmonella Typhi and Ehrlichia species are just two examples. But I am not interested in immune cells.
With fever and thrombocytopenia, I want to know if there is a problem with the red cells.
Hemolysis? Are antibodies coating red blood cells and mediating their consumption by macrophages? Or is hemolysis resulting from abnormal clumps of platelets strung together without fibrin, forming a jagged terrain jutting into the arteriolar lumen and shearing red cells as they stream by? Microangiopathic hemolysis in thrombotic thrombocytopenic purpura.
Is the problem intrinsic to red cells? If not their particular structure, could a foreign pathogen reside within them?
Travel. He had been to Nigeria two months earlier. Although some time has passed before the onset of his symptoms, he is not outside the window for presentation.
The smear was negative for schistocytes but positive for parasites. And his thin smear revealed a density of 0.05%. Clinically, he had no World Health Organization criteria for severe malaria.
We consulted with infectious disease. Speciation was reported as Plasmodium malariae, rather than P. falciparum, and the patient was started on oral antimalarials.
The patient immigrated to the United States years before but frequently visits his home country. His travel history was not prominent during the interview, he did not use mosquito protection measures, and he did not take malaria prophylaxis. After all, he was just going home.