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Diagnosis Deconstructed

Diagnosis Deconstructed: Reflexology to the Rescue

Morchi, Ravi MD

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doi: 10.1097/01.EEM.0000422879.09706.31
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    She is confused and agitated, not complying with anything we ask. Her husband does not know what is going on. She received haloperidol IM multiple times, but we cannot get her compliant for an IV.

    Can she focus on you? Can she pay attention? This is a new change for her, and if she is inattentive now, she is delirious. She does not seem to be responding to internal stimuli, and is not hallucinating as far as we can tell. Her level of alertness is unchanged; she is not lethargic or obtunded.

    Her mental status is not depressed, but acute onset inattentiveness is enough to claim her as delirious, and based on her psychomotor hyperactivity, she has agitated delirium. A medical cause is likely, but what is that cause?

    Vitals. The answer appears to be here at first glance. Room air oxygen saturation is below 90% with rales bilaterally. She reconstitutes to 100% on a non-rebreather face mask and remains that way for the immediate future. But her behavior only gets worse. She was not persistently hypoxemic or hypotensive, and inadequate delivery of substrate could not be blamed for her confusion.

    Glucose. This is normal. This is the substrate most likely to throw otherwise healthy neurons into disarray. But today, serum concentration is not the answer.

    Brain. She has no motor deficit to suggest a vascular obstruction or hemorrhage into the motor strip, corticospinal tracts, basal ganglia, or cerebellum. We know, however, that discrete events in the frontal or temporal lobes can present as confusion without motor abnormalities. Once sedated enough to comply, her head CT will show no new focal abnormality.

    Generalized inflammation of the meninges and the brain parenchyma? Neither a bacterial meningoencephalitis nor a viral encephalitis pattern would later emerge on her CSF studies. Her problem is not infection within the cranial vault.

    Infection outside the cranial vault of necessity would be a susceptible cerebrum. We expect her to have a tattered brain at baseline for cystitis, pneumonia, or another non-CNS infection to cause confusion, one that is atrophic or has multiple hypodensities littered through it, whether by alcohol, a neurodegenerative disorder, or vascular insufficiency. These are the patients we expect to become acutely confused from processes outside their cranial vault in the absence of SIRS criteria. These are the ones in whom we see parainfectious encephalopathy. Her head CT would later show no evidence for chronic parenchymal disease.

    Severe sepsis, with end organ dysfunction being the brain. It is one of the big three, along with decreased urine output and unhappy muscle fibers churning out lactate. A more severe version of a parainfectious encephalopathy, she need not have a lifetime of diseased brain to succumb to this degree of inflammation. An inflammatory cascade that, in addition to altering microvascular tone and inadequately distributing oxygen to neurons, may also poison their mitochondrial machinery. Her heart rate remained elevated at 110 and her lactate returned at 2.9 after a fluid bolus and normal serial blood pressure measurements.

    Vegetables and chocolate sprinkles. She had a crescendo-decrescendo systolic murmur radiating from the apex into the anterior axillary line. I envision endocarditis with pieces of cauliflower flopping atop an incompetent mitral valve. Confusion in these instances may not be simply from rerouting of oxygen or poisoning of mitochondria as in severe sepsis. Rather, her agitation could arise from breadcrumbs of infectious emboli, bacterial conglomerates mixed with thrombus, cupcake sprinkles originating from the mitral valve, shot out of the LV chamber, and drizzled throughout the brain. This may not be apparent on CT or LP. Her extremity exam and conjunctiva revealed no signs of such embolization. Nonetheless, we decided to culture her and cover her for endocarditis.

    Her chest x-ray showed hyperinflated lungs from COPD, and pulmonary edema presumed transudative from new mitral regurgitation. But she did not appear to have the downstream congestion of peripheral nascent pulmonary venules coalescing in interlobular septa with aspirations to later merge with their counterparts medially and form proper pulmonary veins; she did not have Kerley B lines.

    Her emergency department bedside ultrasound demonstrated a thick and dynamic LV with a less vibrant, slightly floppy appearing RV. Her IVC was not a flat pancake that dissolved on inspiration as we see in severely septic patients. Instead it was rather prominent. Still compatible with our diagnosis in this case?

    I thought so. Such an IVC could be seen in new MR and pulmonary venous congestion superimposed on COPD with baseline pulmonary hypertension and RV strain. I did not feel the need to invoke thromboembolus, not with the other cardiopulmonary findings. But she still needed a formal echo to visualize her valves properly.

    So we continued judicious fluids in the hope her RV would have just enough to keep her LV preload adequate but not too much that it flooded her pulmonary parenchyma.

    Worsening agitation despite haloperidol would later be compounded by increased work of breathing and respiratory fatigue, possibly from our iatrogenic acceleration of pulmonary edema. We ended up intubating her.

    Her cardiopulmonary status was impressive, but her cardiovascular status was not. She did not have deplorable sepsis with marginal, vasopressor-dependent perfusion pressures to blame for her outlandish behavior. Her lactate was only slightly elevated, and I could not equate this with any large number of mitochondria halted in their electron transport chain. Her white count was high with bandemia, but her core temperature was normal. I clung to infection mostly because my cupcake sprinkle model of endocarditis invoked direct brain inflammation and so did not necessitate having systemic abnormalities of severe sepsis on which to produce marked confusion. Would this be sufficient in her case?

    Noninfectious encephalopathy. This is broad, ranging from hepatic and renal failure to endocrine gland dysfunction to Lupus cerebritis. Her physical exam revealed no endocrinopathy, and her laboratory tests did not implicate sodium or calcium. Assessment of liver and kidney function did not suggest inadequate disposal of endogenous wastes.

    Reflexology to the rescue. If not endogenous, what about exogenous? Time to move outside the body to find the source. Is everything toxicologic until proven otherwise? I am no toxicologist, but I am versed as a reflexologist. The patterns and groupings of workups we learn to rely on in emergency medicine exist for a reason. I do not advocate a shotgun approach, but I do realize that EP-created order sets have saved more than one case and, in this instance, mine.

    A urine tox screen was ordered because her opening mental status remained disproportionate to any other identifiable medical cause. And, by habit, serum acetaminophen and salicylate levels were included.

    The screen came back positive for cannabis and amphetamines. The acetaminophen level was normal, but her salicylate level was elevated at 57 mg/dl. Sodium bicarbonate was begun in the ICU aiming for the appropriate serum and urine pH goals. She did not have hyperthermia from accelerated metabolic activity. Her original bicarbonate was 13, but she did not actually have an anion gap.

    Could her mental status be attributed to the mitochondrial effects of salicylates? They do not halt the chain like hydrogen sulfide or cyanide; but rather run it to the ground, dissipating heat with little energy production to show for it.

    A formal echo showed her mitral regurgitation was because of a sucking effect of the mitral valve against the interventricular septum, preventing leaflets from coapting while the ventricle was contracting. Termed systolic anterior motion of the mitral valve (SAM), it is secondary to the subaortic Venturi effect created in a narrowed LV outflow tract of a hypertrophic myocardium. No cauliflower seen.

    And her pulmonary edema without Kerley B lines to suggest venous congestion? It very well could have still been from her MR, but I have to say a noncardiogenic component with capillary leak as part of her salicylate toxicity has to be considered.

    It would later be concluded that she suffered from chronic supratherapeutic salicylate intake, possibly compounded by a more acute ingestion. She had SAM and MR from hypertrophy because of longstanding methamphetamine use and COPD from years of smoking. Every facet of her presentation originated exogenously and ran parallel courses on their way to our emergency department.

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