A 90 year old female presented to her local hospital after her family found her to be having difficulty speaking. She was a pretty healthy and active 90 year old. She did have a history of atrial fibrillation and pulmonary emboli and therefore she was on Warfarin.

Upon presentation to her local ER, the physician did find her to have expressive and probably receptive aphasia. Her INR was therapeutic at 2.0. She underwent a noncontrast CT scan of the brain (image above) showing the left subdural hematoma with subfalcine herniation. A Neurosurgical consultation was obtained and the patient was transferred to my NeuroIntensive Care Unit.

The consulting Neurosurgeon was not impressed by the presentation of aphasia and elected to observe her in the ICU. Overnight her aphasia started to improve and then worsen again. A repeat CT showed the same subdural. The patient went to the OR later that day for evacuation.

I was always taught that a subdural hematoma with neurological findings was a surgical emergency. I was confused as to why the Neurosurgeon did not think so. I think I know the answer. Aphasia is not a usual presentation of a subdural hematoma (SDH).

To briefly review, head trauma is the leading cause of SDH usually related to car accidents, falls and assaults. Diffuse cerebral atrophy and the use of anticoagulation round out the list. A seemingly spontaneous unprovoked SDH occurs only 2.6% of the time.

The clinical finding associated with acute SDH is coma in 50% of cases. Posterior fossa SDH presents with symptoms of increased intracranial pressure like headache, vomiting. ataxia. Chronic SDH hematoma usually presents with headache, lightheadedness, apathy and somnolence.

Interestingly in my review, I did not find an aphasia as presenting symptom for SDH. I did find 2 studies- one from the Annals of Neurology which had 4 patients with aphasia and SDH and one form the Journal of American Medical Directors Assocation which had 1 patient with aphasia as a presenting symptom. Having seen this literature I understood a little bit more why the Neurosurgeon was not initially impressed with the case. Next time I will be an even more educated advocate for my patient in terms of needing to go to the OR with SDH presents with aphasia.

Recently I had quite an interesting case. I was very excited about it and I am not sure if that was because it was different than my usual hospital admits or because it is really cool physiology (to me!)

A middle aged gentleman presented to our facility acting confused. His family was convinced he was drunk. He passed medical history included hypertension and a gastric bypass surgery in the early 1970s. On admission, the significant lab findings were an elevated anion gap metabolic acidosis with a normal lactic acid level and without ketones (and a normal alcohol level). His evaluation of this gap acidosis did not reveal any of the usual causes (ie MUDPILES). He was seen by Nephrologist; hydrated with bicarbonate fluid. He recovered and was discharged to home.

He then represented again about 3 days later…with the same thing. Again he had no obvious source of a gap acidosis. He was hydrated with bicarb; improved and was discharged.

About 3 days later, it happened again. This time a different Nephrologist happened to be present for his admission. He said "I think this might be d-lactic acidosis". What?!

D- Lactic acidosis is a unique form of lactic acidosis that can occur in patients with jejunoileal bypass. The mechanism is that glucose and starch are metabolized in the colon to d-lactic which is absorbed into the circulation. D-lactic acid does not respond to LDH and therefore does not get broken down and it builds up in our system. Patients will present with an encephalopathy and they say they "feel drunk". The reason why this becomes an issue in patients with small bowel resection is because usually glucose and starch are absorbed in the small intestine and the colon does not see it. If there is a small bowel resection, the colon sees more glucose and starch and cannot handle.

Another reason why the overproduction of d-lactic acid can occur is due to an overgrowth of gram positive anaerobes, in particular Lactobacilli.

Upon further interviews with my patient, he had been treated as an outpatient for "recurrent" sinus infections and "had been on more antibiotics in the last 6 months then he had been his whole life". As we know antibiotics can lead to an overproduction Lactobacilli. Also he had had his gastric bypass surgery in the 1970s which he said was " a big surgery".

The diagnosis of d-lactic acidosis is made by a special assay. This was ordered on my patient and is still pending.

The treatment of d-lactic acidosis is bicarbonate therapy and antimicrobials to reduce organisms that produce d-lactate. My patient was treated acutely with IV fluids with bicarb and started on Flagyl. He has not been back since which is great for him!
So, there are truly are instances when a patient can look drunk and act drunk but he/she is NOT drunk!

An elderly female presented with a chief complaint of severe right shoulder pain with a "burning sensation" down her arm. In addition she had nausea and vague abdominal
discomfort.

Her past medical history was relatively unremarkable aside from a stage 1A melanoma that had been removed from her left calf about 8 months prior. She had had 2 follow up surveillance visits with her Dermatologist since then and was told that "everything looked good".

Here at our facility she underwent a CT abdomen and pelvis. The image is above. This showed probable diffuse metastatic disease involving the liver, both adrenals and the omentum. There were also two suspicious pulmonary nodules and there was destruction of the right shoulder likely due to metastatic disease.

Malignant melanoma is a potentially devastating disease. The ten year survival rates are as follows: stage 1: 84%, stage 2: 54%, stage 3: 35% and stage IV: 7%. My patient had stage IA disease which has the best survival rate. Having said that, it is well documented that melanoma metastasizes to skin, lymph nodes, the liver, the brain, the lungs and visceral organs. My patient had involvement of all of these areas (aside from skin) on her CT scan.

The patient underwent a liver biopsy of one her lesions. The pathology came back as poorly differentiated adenocarcinoma. This was quite a surprise. The sample was re-stained and evaluated and the conclusion was the same. This then prompted me to do a literature search to see if melanoma is associated with any secondary malignancies. I did not find any literature to suggest that.

The patient has been discharged and is following up with Oncology. Her mammogram, pap smear and colonoscopy were normal.

I question…are we now dealing with an adenocarcinoma of unknown primary on top of a known diagnosis of recent melanoma? Perhaps we are. This is quite an unfortunate outcome for this patient.

Recently I had a young man, who was an AML survivor, present with a triglyceride level of 5800. Usually, my first thought would be that there was a genetic abnormality leading to ineffective cholesterol metabolism. But, I was aware of breast cancer survivors being at risk for dyslipidemia and I began to wonder about leukemics. I then went on a literature search. What I found was quite interesting.

AML has a cure rate of nearly 97%. Therefore, most patients who get it live to tell about it. In terms of what their mortality is after their cure, the literature shows it is divided between heart disease and new malignancies.

In terms of heart disease, they are at risk from dyslipidemia and the metabolic syndrome. Even more interesting is that patients who have had a bone marrow transplant are particularly at risk. In a review article from the journal "Bone Marrow Transplantation"( Majhail et al. June 2008), 86 bone marrow transplant patients were followed. 49% of them were found to have metabolic syndrome. The rate of hypertension and hypertriglyceridemia was significantly higher in them as well. Therefore, I have hypothesized that this young man's high triglyceride level was related to his bone marrow transplant.

The patient and his family ended up calling his transplant center and they agreed that this is a known potential side effect.

I think this case points to the importance of primary care follow up of all cancer survivors. Often cancer patients have to deal with so many issues regarding their cancer that regular primary care issues take the back burner. They take the back burner, that is, until these regular primary care issues land them in the hospital!

A young male patient presented to the emergency room with severe diffuse abdominal pain that had been relentless at home. Prior to this, he had no real medical problems. His CT scan showed severe pancreatitis. He was admitted, started on a PCA as well as fluids. He was kept NPO. A work up was started to look at potential etiologies for his pancreatitis. He did not use alcohol. His gallbladder showed some sludge but no definite stones. He was not taking any medications at home. He had no recent travel or scorpion bites. His metabolic panel including electrolytes was all normal. THEN, his lipid panel came back. His triglyceride level was 5880.
Hypertriglyceridemia accounts for only 1.3-3.8% of pancreatitis attacks according to recent medical data. Even then the likelihood of having a triglyceride level over 1000 is rare. It occurs in 1 in 5000 people.
This case raised a question for me: how do we start lowering his triglycerides when he needs to be on bowel rest for his severe pancreatitis? I posed this question to our Gastroenterologist. The answer was quite interesting. He said that just by being NPO the triglyceride level would start to naturally trend down, not to normal, but down to a level where the pancreas would recover. Then we would initiate the oral agents along the a very low fat diet in order to control his levels.
The most fascinating thing was that on hospital day #2 his triglyceride level had already dropped to 2700! The patient started to have a slow resolution of his abdominal discomfort.
Hypertriglyceridemia is a rare but definite cause of pancreatitis and when it hits it certainly does make itself known! The patient said to me "I guess this means no more Big Macs!" I guess so!

A 60 year old male with a known history of metastatic renal cell cancer was transferred to our hospital with an intracerebral hemorrhage. He had known metastatic disease to the brain and developed a DVT. He was started on Lovenox for anticoagulation and proceeded to bleed into one his brain lesions. I thought this posed an interesting question about what is the evidence regarding anticoagulation in the setting of brain mets.
The current recommendation IS to anticoagulate DVTs in the setting of primary brain tumors and metastatic disease that has a low propensity to bleeding.
In order to discern which metastatic diseases have a low propensity to bleed, it is easier to state which have a HIGH propensity to bleed: melanoma, choriocarcinoma, thyroid carcinoma and renal cell carcinoma. If a patient is suffering from brain metastases from one of these conditions and develops a DVT/PE, the recommendation is to not anticoagulate these patients and to place a permanent IVC filter. Some authors have stated that if there is a single brain lesion associated with one of the above cancers and that lesion is resected and the person develops thrombosis then aspirin should be used.
In the above mentioned patient, the literature would not have supported anticoagulation in this patient. In the end, this patient did received a permanent IVC filter. He does have some visual field defects associated with his cerebral hemorrhage.

When I was in residency, my favorite Nephrologist told the story of his patient with chronic kidney disease who had "killed himself with V8 juice". The patient had been instructed a number of times regarding the potassium present in V8 but he liked it and did not want to stop drinking it and he eventually passed away with hyperkalemia.
I was reminded of this story recently when I was called to a code. There was an elderly male who was on our rehab floor who had the sudden loss of consciousness and pulselessness. CPR was started and the monitor showed persistent asystole. While the code was running, I was able to quickly scan through his chart and see that his creatinine had been rising and he had been on potassium supplementation three times a day and his potassium had been elevated that morning. I quickly have calcium, dextrose and insulin. He regained a rhythm and pulse and was transferred the ICU.
Hyperkalemia is known to cause cardiac conduction abnormalities. The usual progression is peaked T waves with shortening of the QT interval. This followed by progressive lengthening of the PR interval and QRS. The P wave eventually falls and the rhythm goes to asystole or ventricular fibrillation.
Whether is it V8 ingestion or iatrogenic potassium supplementation, we need to remember to be very careful with the potassium level in patients with renal disease.

Recently a women in her late 40s presented to our hospital with a complaint of reduced exercise capacity and "heavy legs". Her only medication was her birth control pill. Her evaluation revealed a large thrombosis that orginated in her IVC just below the level of the renal veins and extended down into both of her femoral veins.
It is well documented that oral contraceptive pills (OCPs) increase the risk of thrombosis in women. Oral contraceptives are one of the most commonly prescribed pills the world and I think it is worthwhile to review what the risk of thromobis is.
There is no hard and fast data to say exactly how much OCPs increase the risk of thrombosis. Hematologists I have spoken with say that there is an increased risk that increases with age. Obviously there is an even greater risk in women with thrombophilia. Meanwhile there is certainly no evidence that every women who wants to use an OCP should have laboratory testing for thrombophilia. We also know that this risk increases with tobacco abuse.
Of course there are also many benefits of OCPs including desired birth control and reduction in ovarian cancer.
Overall I think we need to be reminded to advise our female patients of the risk of thrombosis with OCPs. We need to do a thorough personal and family history to look for anything that might suggest a thrombophilia. We should also be ready to investigate these women when they complain of anything that might suggest they have developed a thrombus.

I met my 55 year old patient as she was coding... again. My partner had seen her in consult for vent management prior to my shift. She had no medical problems aside from tobacco abuse and had been lifting a snowblower up into a truck when she had the sudden onset of chest pain and then she lost consciousness. Her family did CPR for 5 minutes; an outide hospital gave TPA for her STEMI(ST elevation myocardial infarction). Upon arrival at my hospital she had gone for cardiac cath where her LAD was stented. Her post-cath EKG was beautiful and now she was coding again.
And code she did for 75 minutes. She was between v fib (ventricular fibrillation) and PEA (pulsless electrical activity), I think. I say "I think" because I could not feel her pulse and we had to doppler her carotid. Her EKG showed new infarction. She went to the cath lab again. She continued to code in the cath lab for another 80 minutes. Despite a balloon pump and maximum pressors, her systolic BP did not go over 50 for HOURS. I thought for sure she was going to die.
The Cardiologist transferred her to the CVICU for her family to be with her. The thing is that she did NOT die. Slowly over the next 48 hours she was weaned off the balloon and pressors and extubated. She woke up and she appears without neurologic deficit.
I am totally humbled by her survival. The only way I am able to wrap my mind around it is to think that CPR saved her life. This reenforces that AHA recommendation for CPR only CPR. It works. It worked for this patient. She was truly given an early Christmas present!

Recently I had the opportunity to read, Dr. Sanjay Gupta's "Cheating Death". Overall I thought it was good but I think it may have been intended for lay readers in lieu of health care providers. There was a significant portion of the book spent on explaining various medical conditions and procedures that sometimes got tedious. Also there were chapters spent on hypothermia and suspended animation that I think might lead readers astray. The hypothermia chapter talked about the cooling process of cardiac and stroke patients at Columbia University in New York. As you can imagine at Columbia, they tend to be ahead of the research and doing protocols that most mainstream community hospitals (like I work at) are not pursuing. I think this can give laypeople a false sense of normalcy regarding the treatment of these medical conditions. I am not saying that we do not cool our cardiac patients but I do not think we do it at the level of Columbia.
There was one chapter in the book that I did find particularly interesting. It was the chapter on Near Death Experiences. That is not something you usually read about in the New England Journal or the Annals. Anyone who was fainted knows what it feels like to be there one second and gone the next. What I find fascinating are the levels of consciousness and how much we do not know about them. I have had a number of patients who are "near death" tell me that they see their dead spouse or sibling etc. I always tell the patient's families not to worry when the patient says these things because really how do we know that they are not there?