“Watson! Pull down that window. The cacophony of the London Street does little to enhance the sound of my violin playing.”
I rarely talked back to the world’s greatest detective, but I had to bite my tongue, because I wanted to say: “Holmes, the street’s music rather soothes the strains of your instrument’s cacophony.”
“My music is not meant to soothe you into a sea of self-indulgence.” He seemed to read my mind. “I play the musical patterns in my head…which may seem a dissonance to you, but to me, the notes create a pattern that has a sweet simplicity of order.”
A rapid fire knock at the door broke into our discussion. An old colleague from medical school, rushed into the room, more tousled and frazzled than I had ever seen him.
“Watson, dear Watson, I need your help now more than ever. I have a case that is eating me alive. I cannot make heads or tails of it all.”
“Sit here,” I offered him a chair, “and give Holmes and I all the details from the very start of the conundrum.”
The Beginning
The Case
THE FIRST SHOE FALLS OFF
“The urine culture came back showing ESBL E. Coli infection. It was sensitive to two oral antibiotics: Augmentin or Nitrofurantoin. I chose Augmentin given his prostatitis and avoided Nitrofurantoin due to notorious bad prostate penetration.
His vital signs remained stable and he seemed to perk up for one day, then he became a disaster. He had a massive GI bleed with bright red blood per rectum. He became hypotensive and unresponsive to IV fluid. He wasn’t just septic with ESBL, he was in DIC.
Hemoglobin: 7
HCT: 23
Platelets: 229,000
PT/INR: 2.5
Albumin: 1.2
BUN/Cr: 36/.8
“I started him on IV Meropenem, and gave him two units of FFP to provide clotting power. I transfused him with two units of PRBC. He tolerated the transfusions well, but I had to place him on three different pressor agents to keep his BP at 80/60. Central lines, arterial line, and lots of blood, sweat, and tears went into the mix.”
Holmes opened his eyes and pressed his fingers together, a sure sign that he was now interested in the case.
CTA Abdomen: No compelling evidence of active gastrointestinal bleeding.
“The patient’s bleeding stopped and his H and H stabilized. The pressorscame off, step by step, and he stabilized his BP at 120/70. The GI consultant was fearful of doing a colonoscopy unless the patient had further GI bleeding, which he did not have.”
MBSS: severe aspiration of all textures
“Given the patient’s severe risk for aspiration of oral nutrition, and given his malnourished state and low Albumin, a PEG tube was placed for enteral nutrition. For the first time in weeks, I sensed that the patient was out of the woods. Mr. Holmes, I couldn’t have been more mistaken.”
THE SECOND SHOE FALLS OFF
“The patient was started on continuous feeds with Osmoliteat 25cc/hrand when well-tolerated for 24 hours, advanced to 50cc/hr, supplying him with 1800 calories per day and 1600cc of fluid, including tidtube flushes.
I was so tickled at his progress that I arranged for transfer back to his home. The patient’s providers preferred bolus feeding through the PEG tube, if I felt that this was a reasonable alternative. I wrote the order for bolus feeding, starting low and moving slow. I had a PICC line placed for his daily Meropenemdose, as no further IV fluids were needed.
However, that very night he dropped his BP into the basement. The BP graph looked like this for the next few days”:


More Labs
The Second Shoe Falls Off
The Solution
The Final Word
“Patterns, Watson. If you have a clinical head-scratcher, plot a graph and look for patterns. Perhaps this is a good time for a musical pattern or two that I will scratch out on my violin.
Sources
Doyle, Arthur Conan; The Adventures of Sherlock Holmes, 1893
Sato, Koichi; Postprandial hypotension in older people receiving tube feeding through gastrostomy: Tube feeding and postprandial hypotension; August 2018; Geriatrics & Gerontology International18(10)
HISTORY
“My patient is a 93 year old male, a friendly, dear man with a touch of dementia, who stopped eating two weeks ago and became rather listless. He always had a robust appetite and a fair ability to move about, so the change was quite abrupt. He had no fever, no emesis, no diarrhea, no coughing, no trouble breathing. He denied pain of any sort. He had no falls, no new stresses, nor changes in his medical regimen.”
His history is significant for hypothyroidism, but a recent TSH showed him quite euthyroid. He does have a history of Hypertension, well controlled with Losartan, 25 mg daily, and a minor CVA from which the patient had recovered completely. He takes a baby aspirin daily.
EXAM
His BP had been stable for weeks at 134/78. His pulse was 70-80. His pulse oximetry was terrific at 97% on room air. The rest of the exam:
HEENT –normal
LUNGS –clear
HEART –no murmur, regular rate
ABDOMEN –soft and nontender
EXTREMITIES –dry and warm with no edema and good pulses
NEURO –unremarkable
PROSTATE –tender and boggy
HEME –negative
GENITALIA –no hernia
LABS
Urinalysis: cloudy with trace protein, positive Nitrites and TNTC WBCs.
“I cultured the urine and started my patient on Ciprofloxacin, a reasonable oral antibiotic for E. coli Prostatitis, using the typical community sensitivities as my guide for empiric coverage.”
CBC –normal
Bun/Cr –normal
Liver enzymes -normal
Holmes yawned without the tiniest attempt to cover it from our guest. “Another scintillating case of Acute Prostatitis in an old man. Are all the great cases gone forever from the clinics of London?” Holmes repined.

“I warned the family that that patient was nearing the end of the road. I had done all that I could do, within reason. I explained that his hemorrhagic and septic shock had taken too high a toll on his body. He was leaking every cc of fluid that I put in him into his skin. He looked like a sloshing bag of water. His skin literally wept fluid day and night. He soaked sheets with fluid leaking from every pore. His Albumin was so low and his Oncotic pressure so pitiful, that he couldn’t maintain his BP and would surely soon lose kidney function, spill fluids into his lungs, and drown in his own juices.”
Holmes was intently studying the BP graph with his trusty magnifying lens, perhaps more for show than for any true need. He always had a flare for the dramatic. “May I see the hospital records that you have so kindly brought for my perusal?” My colleague handed the bundle of papers to Holmes, who rapidly flipped through page after page of SOAP notes and orders and results.
“My dear man,” Holmes began, “stop those bolus feeds and your patient will soon be at home, in the safe harbor of a loving family.”
“You amaze me, Mr. Holmes,” my colleague stared at the detective, “could it be that simple?”
“Not could, old man. It is.”
THE SOLUTION
After my colleague had left our rooms at 21B Baker Street, I turned to Holmes: “Are you so sure, Holmes? A precious life hangs in the balance on your word and you never have laid eyes on the patient.”
“My eyes see what you practitioners don’t see. Patterns, Watson, patterns. They are my life’s blood.”
“The patient’s hypotensive episodes could only be explained by three things,” he continued. “Worsening sepsis, Aspiration Pneumonia, or a less benign factor. First, please consider worsening sepsis due to antibiotic resistance. The patient’s temperature curve is singular and telling:


“At the patient’s advanced age, hypothermia, rather than hyperthermia, is not infrequently the sign of severe infection. Notice that he presented in septic shock and hypothermia. Once he was stabilized, his temperature normalized and he did not develop further hypothermia, despite the episodes of hypotension. Now, Watson, look at the White Blood Count graph:


“Watson, there is no evidence that the patient’s infection was rearing it’s ugly head. He had no hypothermia, his WBC supported the clinic picture that the patient was no longer septic. In fact, the repeat Urine Culture was negative. Gone was the ESBL bacteria from his bladder. His hypotensive episodes were not due to recurrent sepsis.
Were the recorded hypotensive episodes due to Aspiration Pneumonia?
Let us peruse his chest x-ray:
His prior CXRs showed increasing atelectasis, pleural effusion, and pulmonary edema –easily explained by the many litresof Normal Saline and FFP and blood products that he had received. Besides, the poor fellow had been on broad-spectrum antibiotic coverage for days, easily covering any anaerobes which dared tried to get into his lungs. And we have proved that his clinical and laboratory picture did not fit sepsis.” He cracked his knuckles and gave a familiar chuckle.
“Look at this graph, my friend”:


“The B = bolus feeds, the C = continuous feeds.” Holmes sat back in his chair and smiled. “In the elderly, nearly 75% of patients have hypotensive episodes after a bolus PEG tube feeding. It is common, not deadly, but very disturbing to the uninitiated. The answer was elementary once I looked back at the timing of his PEG bolus feedings and his episodes of hypotension. The solution was simple: return the patient to continuous feeds, change the feeding solution to one with less glucose, like Glucerna, and sit back and watch him thrive.

“Patterns, Watson. If you have a clinical head-scratcher, plot a graph and look for patterns. Perhaps this is a good time for a musical pattern or two that I will scratch out on my violin.

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