Skin deep

There are only a few true dermatological emergencies, but skin problems are a common cause of ER visits. Red, scaly, itchy, painful, blistered are all part of the skin game.

Toxic epidermal necrolysis is a life threatening skin problem. It is seen in Steven-Johnson syndrome, a hypersenitivity reaction that may be caused by many commonly used medications. The skin and mucous membranes are effected and the treatment is similar to that for severe burns. Scalded skin syndrome, caused by certain staphylococcal infections is characterized by fluid filled blisters as the outer layer of skin separates from the deeper layers. This separation with only slight pressure is referred to as Nikolsky's sign. This condition is also treated in a burn center.Pemphigous is an autoimmune disease that also presents with painful blisters. It may be associated with certain cancers.

Skin infections are often seen in the ER. Fungal infections of the skin are caused by dermatophytes. Ringworm, athlete's foot, and jock itch are all common names for fungal skin infections. Tinea versicolor presents with patches of of skin that are a different color than the normal surrounding skin. Tinea pedis, pubis and capitis refer to fungal infection from the bottom, middle and top of the body. While not life-threatening, the ER docs and PA's can initiate treatment for these conditions.

Viral skin infections are potentially more serious. Herpes infections caused by herpes simplex either types 1 or 2 are painful eruptions of small blisters (vesicles) around the mouth or genitals. Occasionally a herpetic whitlow presents as painful vessicles on a finger tip from the patient contaminating his or hers finger from touching/scratching vesicles around the mouth or genitals. Shingles is caused by the herpes zoster virus. This virus is also the cause of varicella (chicken pox). Many species of herpes virus have the ability to "hide" in ones body and recur years after the initial infection. Shingles describes a recurrence along the distribution area of a nerve. It is almost always unilateral and looks like a patch or swath of vesicles on a red base. The incidence of shingles increases as we age. It is a very painful condition and the pain often persists even after the rash clears. Fortunately there a booster vaccination for patients older than 60 that has been shown to decrease the incidence of shingles and to both shorten the course and the postherpetic neuralgia (nerve pain) if shingles does occur.

Many diseases have distinctive rashes as part of the illness. Measles, chicken pox, rubella, Rocky Mountain spotted fever, Lyme disease and many other viral and bacterial infections will have rashes as part of the signs of the illness.

Bacterial skin infections are common and need urgent treatment. Erysipelas is a painful skin eruption caused by strep. pyogenes. Impetigo is a common childhood skin infection caused when scratching by the patient, breaks the surface of the skin and strep or staph bacteria are inoculated into the skin. Impetigo is often seen in sports where skin to skin contact occurs, such as wrestling. Cellulitis presents as a localized red, warm and tender skin. The margin of the cellulitis is often elevated above the normal skin. Staph and strep bacteria are the most common organisms. Impaired immunity because of medications or diabetes increases the incidence and severity of cellulitis.

By far the most common dermatological conditions seen in the ER are those caused by inflammation. Contact dermatitis by irritants such as solvents, alkalies, latex and plants presents with area of small vesicles, sometimes "weeping". Allergic dermatitis looks similar and is most often seen with exposure to poison ivy, oak, sumac and metals such as nickel. That gold or silver jewelry you are wearing may contain nickel as a hardener. Photodermatitis occurs when an irritant or allergen is on the skin or has been ingested (many medications) and the ultraviolet light from sun exposure triggers a reaction.

Eczema is a chronic form of dermatitis that may present with some combination of redness, itching, dryness, crusting, flaking, blistering, cracking, oozing or bleeding. Eczema like contact dermatitis is treated with topically applied or orally administered corticosteroids.

Psoriasis is a chronic immune mediated skin disease. Thick flaky patches may occur anywhere on the body. Topical steroids may help with an acute flair up. PUVA (psoralens and ultraviolet A phototherapy) and immune modulators such as methotrexate or cyclosporin are used to treat this chronic condition.

Patients with sunburns are frequently seen in the ER at this time of the year. Moisturizers, pain medications and occasionally corticosteroids are prescribed. Prevention by limiting ones exposure, and using sunblock are the preferred method of not getting burned. Apply copious amounts of at least SPF 30 sun block, twenty minutes before sun exposure. Reapply every 2 hours or more frequently if swimming or sweating. As I found out on while snorkeling on the island of Anguilla, remember to protect ones bald spot.

World's oldest ER doc update: I have begun the next phase of my ER career. I am now working at a low volume/ low acuity community hospital. Although this move was forced on me by the adminstration of my former hospital, the slower pace and reduced stress will allow me to reach my goal of 40 years as an ER doc.

Last Dance

This is it. Last night at LGH. 28 years. I have mixed emotions. LGH was more than a job. My family and I were all treated as patients in this hospital. My father-in-law died here. I made friends who have proved tried and true in my times of need. I have worked with and treated generations of people at LGH. The current administration felt that I needed to leave. I will join a list of nurses, techs, aides, and secretaries who were also shown the door. The criteria for hiring and firing people seems to have more to do with personality conflicts than competency. The upside of leaving is a blessed lessening of my stress level. The lack of space and personnel relative to the volume and acuity of our patients, has made this ER a risky place to be a worker or a patient.

There are kind, smart, hard working nurses, doctors, physician assistants, techs, and support staff. They will provide our patients with very good, if slow care. They deserve to be recognized by there leaders for the extraordinary work that they do. Good luck to all my friends.

A special thanks to Sue G, Deb, Sandi, Kristen, Jess, Fo, Donna S, Marie P, Donna B, Jackie, the Rachels, Heidi, Bubba, Lisa B, Leza, Kellie, Dawna T, Mel, Brandy, Tara and all the folks on nights. I will miss my partners. I leave the night shift in the strong hands of my brother, Chris K.

The world's oldest ER doc will continue to blog but at a new lodge of the B.O.N.E.R. docs

Lyme Disease

Time to walk the dog. Hot and humid conditions but I don a long sleeve shirt treated with insect repellent and long white pants. I tuck the cuffs of the pants into heavy white socks. Why? Ticks!

Deer ticks of the genus Ixodes may transmit Lyme disease with a bite. A spirochete (spiral shaped bacterium), Borrelia burgdorferi is the causative organism. The tiny deer tick must be attached for at 36 hours before transmitting the pathogen. In the ER a single dose of antibiotic may be given if the tick bitten patient meets certain criteria. Most important is that the tick is identified as a deer tick and not the more common dog tick. The deer tick must have been attached for at least 36 hours and the antibiotics be given with 72 hours of removing the tick. The preferred antibiotic is doxycycline. For children, women who are pregnant or breast feeding, or those patients allergic to tetracycline, another antibiotic will be used.

Early Lyme disease is characterized by flulike symptoms. The patient often has chills, a low grade fever, headache, muscle aches, tiredness, joint aches, and less frequently nausea and vomiting. These symptoms appear within 30 days of the initial bite. A characteristic rash, erythema migrans (EM), occurs in 80% of Lyme disease patients, on average 7-10 days post bite. It is flat and red and spreads out from the center. 40% of the cases of erythema migrans show clearing of the redness staring in the center and moving to the edges. 20% of patients with EM will have separate lesions, thought to be from spread of the bacteria via the blood stream.

Stage 2 Lyme disease is also referred to early disseminated. Neurological, joint and cardiac manifestations of Lyme disease are present. Cardiac problems occur in less than 10% of stage 2 and 3 Lyme patients. Palpitations, syncope (sudden loss of consciousness) and chest pains are the symptoms of borrelia infection of the heart. Damage to the conducting cells in the heart may lead to dangerously slow heart rates. Infection with inflammation of the heart muscle and/or the membrane covering the heart chest pain from myocarditis or pericarditis respectively.

Joint pains or arthralgias are common in both stage 1 and 2 of Lyme disease. Actual inflammation of the joints, arthritis is more commonly seen in stage 3. Bursitis, myositis, sinovitis, and tendonitis causes pains of muscles, tendons and bursae.

Infection of the cornea or uvea of the eye may lead to eye pain and visual changes in some Lyme patients.

Stage 2 disease occurs weeks to months after the initial bite. The neuropsychiatric symptoms of stage 2 Lyme are varied and mimic other diseases. Decreased concentration, memory disorders, numbness, nerve pains, sleep disorders, paralysis of facial muscles and visual changes have all been reported. 25% of Lyme patients with a facial palsy will have the condition on both sides of the face. Headache and neck pain and stiffness are symptoms of Lyme meningitis.

Other signs of Lyme disease may include an enlarged liver or spleen and enlarged lymph nodes. Blood tests starting with the ELISA for Lyme will be sent. A Western Blot test may be used to confirm the diagnosis. A lumbar puncture will be done if there are signs of meningitis or neurological symptoms of Lyme disease.

Stage 3 Lyme disease, or tertiary Lyme occurs months to years after the initial bite. This may happen because the initial disease wasn't treated at all or inadequately. There is some experimental evidence that the spirochete may persist intracellularly in fibroblasts despite adequate antibiotic treatment. Arthritis of the knees and other large joints is evident in tertiary Lyme. Cardiac symptoms as noted earlier are also occasionally found in stage 3. Fatigue, chronic headaches, memory loss, sleep disorders, abnormal sensitivity to light, confusion, decreased levels of consciousness and numbness and tingling are all neurological signs of tertiary Lyme disease.

Chronic Lyme disease is reported by some patients. This may represent an autoimmune phenomenon. Molecular mimicry occurs when one's immune system attacks one's body because of similarity to molecular components of the Borrelia spirochete. Some physician treat chronic Lyme patients with antibiotics for many months to years. There is no experimental proof that this treatment is effective.

As with many of life's unpleasant diseases, prevention is the best weapon. Risks of exposure to deer ticks are gardening, hiking, hunting, walking in high grass and pet ownership. My bizarre attire when dog walking is just what is recommended. Long sleeves and pants. Insect repellent sprays. Light colored clothes to more easily spot the tiny ticks. Use of tick and flea treatments for outdoor pets is also a good idea. There is a veterinary vaccine for Lyme but its effectiveness is questionable. Have a great summer.

E Coli

Scary stories about E coli outbreaks appear in the news regularly. The most recent occurrence in Germany is worrisome because of the deaths of younger healthier women and the lack of an obvious source.

E coli is a resident bacteria of the human GI tract. One's personal inhabiting specie rarely causes problems. The proximity of the rectum and vagina in women make E coli a common cause of urinary tract infections. E coli may infrequentlt cause pneumonia and meningitis in neonates, long-term care residents and hospitalized patients. The bacteria may infect diabetic and decubitus (pressure sores) ulcers and causes up to 10% of bacterial bone infections in the vertebrae. The newsworthy danger arises when one is exposed to a strain of the bug that produces toxins that cause harm to the human host.

The most familiar of these toxin producing strains of E coli is the enterotoxigenic variety. Euphemisms such as traveler's diarrhea or Montezuma's revenge make the illness seem trivial. Bouts of watery diarrhea are no fun. Treatment however is relatively simple; rehydrate with fluids and Pepto Bismol in large quantities.

STEC/EHEC refers to strains of coliforms that produce a Shiga toxin. Shigella bacteria are another cause of gastrointestinal infection. The shiga toxin invades the lining of the intestinal tract and enters the blood stream. Unrelated species of bacteria may "share" genetic material by exchanging plasmids. Plasmids are packages of genes that may encode for resistance to antibiotics or production of a toxic protein.

Shiga toxin targets the endothelial cells that line blood vessels. The resulting damage is referred to as microangiopathy. The red blood cells and platelets (clotting cells) are injured as they pass through the damaged blood vessels. Hemolytic anemia (low RBC's from lysis or rupture) and TTP (low platelet counts from consumption of the platelets in clotting) cause the life-threatening consequences of HUS, hemolytic uremic syndrome.

The kidneys main function is filtering out toxic products from metabolism. They are highly vascular. In the kidney cells, the Shiga toxin inhibits protein synthesis, eventually leading to apoptosis (cell death). The lysis of RBC's, the direct damage to renal blood vessels and renal cell apoptosis may lead to kidney failure, i.e. HUS. If recognized early, intravenous fluids may prevent renal failure. Once established, renal failure is treated with hemodialysis until the kidneys recover. The kidney failure may be permanent and lead to a life of thrice weekly dialysis while awaiting a kidney transplant.

The early symptoms of STEC/EHEC are bloody stools, fever, lethargy, vomiting and weakness. Diarrhea, vomiting and increased irritability may be the only early symptoms in babies. Later in the course of the illness, patients may have bruising, decreased level of consciousness, low or no urine output, pallor, petechiae (small red or purple skin lesions) and jaundice. HUS is most common at the extremes of age. The very young and the elderly are usually most at risk.

In the USA, outbreaks of HUS from enteroinvasive strains of E coli have come from contaminated meat (especially hamburger) and vegetables contaminated by irrigation water that had been fouled by animal waste. Thoroughly cooking meat eliminates the risk but washing vegetables does not. There have been proposals to irradiate food products to kill the bacteria in and on the food. Irradiation does not make the food radioactive but it may alter the taste or texture of the food.

The most useful thing that we can all do to prevent the spread of food borne illnesses is good hand washing. Fecal-oral spread sounds gross but is all too frequently the source of both viral and bacterial gastroenteritis. Reminding children to wash their hands after going to the bathroom is a must. I have been tempted to expose people that I have seen leaving public bathrooms without washing their hands.

Use warm water, soap, and scrub for at least a minute, use paper towels to dry your hands and also to shut off the water and open the door. Any ground meat must be cooked completely. A hamburger with a red center is a "crap" shoot.

Cramp Champ

After 33 years of being an ER doc, I had a first time chief complaint. A 60+ year old patient came to the ER around 0400 complaining of painful leg cramps. The patient reeked of Ben-Gay and it took a great deal of control, to not start laughing at the less than urgent nature of the patient's problem. As an example of Karma, I spent my first not at home (after my usual three 10 hour nights from hell) walking around the house trying to relieve my own painful calf and foot cramps. I especially hated the fact that my left big toe was painfully sticking up like a flag pole.

Leg cramps, aka Charley horse, are not restless leg syndrome. RLS is a movement disorder that is treated with meds for Parkinson's disease. Although RLS is uncomfortable and may be associated with some muscle cramping, it is not nocturnal leg cramps. Cramps are painful contractions of the thigh, calf and/or foot muscles.

Any athlete will recognize the painful muscle cramping that occurs during or immediately after heavy exercise, especially in hot weather. Dehydration, electrolyte loss through sweating, and the build up of lactic acid in the muscles from anaerobic metabolism can lead to these painful muscle contractions, sometimes referred to as heat cramps. When the diaphragm is involved the dolorous spasm may be called a "stitch".

Nocturnal leg cramps have been linked to sitting for long periods of time, dehydration, overuse of the muscles, standing or working on concrete floors and a number of medications. The list of prescriptions medication includes diuretics, statins, lithium, and morphine. The incidence of nocturnal leg cramps increases with age and is occasionally associated with diabetes and peripheral vascular disease and infrequently with endocrine disorders such as hypothyroidism and hypoglycemia.

There is no well established treatment for nocturnal leg cramps. Good hydration, stretching of the calf muscles before bed, having loose bed clothes and linen, even riding an exercise bike have been proposed as preventatives. Eating potassium rich foods, such as bananas and oranges is recommended. Drinking water before bed may be helpful but, will lead to another night problem for men in my age demographic.

Quinine is a medication that was (and sometimes still is) used to treat malaria. As a doctor back in the 70's, many of the elderly patients that I treated were taking quinine nightly to prevent leg cramps. There is no double blind study that definitely shows improvement in the frequency or intensity of leg cramps by taking quinine. Anecdotal reports have perpetrated the continued use of quinine for this condition. My patient had taken quinine sulfate when he was awakened by his painful cramps. The down side of quinine is significant. Side effects include headache and tinnitus (ringing in the ears), thrombocytopenia (low platelet count), cardiac rhythm disturbances, and fatal hypersenitivity reactions.

Diltiazem, a calcium channel blocker used to treat hypertension and rapid heart rates, has been tried with some success to treat nocturnal leg cramps. Vitamin B6 30 mg daily has also been proffered as a treatment option. Neither has been subjected to a well controlled study.

So it is 3 AM and you are awakened by painful cramps in your lower extremities; what do you do? First, get out of bed and begin to walk around. Drink some water. Gently massage the involved muscles. Take a warm shower or bath. Do some stretching of your calves.

If you are plagued with frequent nocturnal leg cramps, talk to your primary care doctor. A check of your electrolyte levels, thyroid function and possibly even EMG (electromyelography) may be helpful in finding a treatable cause.

Update on my status: I have 12 shifts left at the General Hospital. Working another Sunday- Tuesday for the Memorial Day Weekend, will reinforce the need to find greener (less stressful) pastures. The new night shift at The General will commence in June. The hours will be 10PM to 6AM. I have nine of these truncated shifts before my final night on June 25. I will begin my new job around July 18th. My schedule will be 11PM to 7 AM working 12 shifts per month. The night shift census is 4-6 patients. I have been averaging 25 patients per 10 hour night at The General.

APAP

APAP is short for acetaminophen, the active ingredient in Tylenol and Feveral. APAP is used to treat fever and pain. It is found as a single drug and in combination with other medications in cold and flu treatments. I touched on APAP in a prior post titled OD. A recent patient and a memory from the past led to today's blog.

APAP toxicity is primary from injury and death of hepatocytes, liver cells. NAPQI is a metabolite, an altered form of APAP as is metabolized by the liver. NAPQI depletes the liver's store of glutathione, an antioxidant. Once the supply of glutathione is exhausted, the hepatocytes are unable to repair the damage caused by NAPQI. Alcohol and medications that use the same pathway for liver metabolism, will exacerbate the toxic effects of APAP. Isoniazid, which is used to treat tuberculosis, and phenobarbital and carbamazipine, both anticonvulsants, are in this group of medications.

In an acute overdose of APAP, either as a suicide attempt or inadvertent excessive dose given by a parent, well established toxic levels are predictable. 200 mg per Kg of body weight is enough to cause liver damage. The level of APAP at 4 hours after a single ingestion can be plotted on the Rumack-Matthew nomogram to help the ER doc decide if the patient requires treatment. Many times we see patients who have been taking excessive amounts of APAP over days. The nomogram is not helpful in these patients.

The early signs of hepatic injury from APAP are not very specific. The patient may have some right upper abdominal discomfort and complain of nausea and vomiting. As the liver is crucial for the maintenance of glucose levels, low blood sugar may be found. Easy bruising is also a sign of liver injury, as the liver manufactures proteins involved in the clotting of blood. As the levels of nitrogen containing toxins, such as ammonia, build up in the blood, the patient may show signs of hepatic encephalopathy. Confusion, problems walking, and lethargy are all signs of effects of these toxins on the brain. A healthy liver normally clears these products of protein metabolism and absorbed toxins from the gastrointestinal track.

Lab tests will reveal elevated liver enzymes, transaminases. Bilirubin may be above normal and later in the course of the disease, abnormal kidney function will be noted. The prothrombin time, a measure of the clotting cascade will begin to rise. The key to a successful outcome is to initiate treatment as soon as possible, preferably before the patient is in significant liver failure.

N-acetylcysteine or NAC is the antidote for APAP damage to the liver. There is an intravenous form of NAC that is sold as Acetadote in the US. Prior to its introduction, NAC had to be given orally. This was a problem because the patients often had vomiting from liver injury and the oral form of NAC smells like rotten eggs. If liver failure has progressed too far, only a liver transplant will save the patient.

Early in my long career, I examined a toddler who looked gravely ill. The child was jaundiced, dehydrated, unresponsive and bled excessively from attempts to establish an IV and draw blood. The lab tests showed all the signs of liver failure. I began NAC by a nasogastric tube as the IV form was not available at that time. The child was transferred to a major pediatric hospital but died from liver failure. The child had been treated for a viral infection with APAP by the parents. The pediatrician had told the parents to give one teaspoon of children's APAP, which contains 160 mg of the drug, every four hours as needed for fever. The problem arose because the parents mistakenly gave one teaspoon of infant APAP, which contains 500 mg, every four hours.

More recently a patient was seen in the ER who was taking more than the maximally recommended dose of APAP for chronic pain. The doses taken were 25-33% above the maximal dose but over many days the liver began to be effected. This patient was started on Acetadote and made a full recovery.

Update:

My mother-in-law is, in the words of the hospice nurse, actively dying. She is unresponsive and hasn't had any oral intake in several days. We are amazed that she is still alive. My wife and I are with mother as I write this post.

The next phase of my career will begin in July. I will be leaving the ER I have called home for the past 28 years. My departure was forced by the hospital administration's displeasure with my relationship with the nursing staff. The outpouring of support from current and former ER nurses, my colleagues in the ER and on the medical staff, EMS personnel, local police officers and firefighters, and my patients has been heartening.

I have decided to remain a B.O.N.E.R. doc. I will stay on nights but in a much less busy ER. The privilege of providing care to those most in need, is my motivation. Stay tuned.

April Fool's Day

As I write this posting, I am looking out at several inches of heavy snow. April Fools indeed. The ER is a place where pranks occur almost daily. The odd, unexpected, quirky and bizarre arrive by foot, wheelchair and ambulance stretcher. The intentional April Fool's day prank are rare and amateurish. Painted on rashes and fake aliens erupting from the body are not going to fool the world's oldest ER doc.

It is the unintentional gag that makes the job fun. Many years ago I was confronted with a mother dragging her 6 year old into the ER screaming that he couldn't breath and was turning blue. A quick glance revealed a smurf like coloration of the hands and face but the child was breathing calmly. I pulled an alcohol wipe from my coat pocket and removed the blue dye that had bled from the child's new sweatshirt. The mother's mouth gaped and she left the ER without saying another word. The rare and unexpected finding keeps me on my toes. When I have completed a history and physical exam and reviewed any records in the hospital's EMR, I form my differential diagnosis. The labs, x-rays, CT's, EKG, and ultrasound should yield findings that I hope I have anticipated. The patient with crushing chest pain and difficulty breathing, who is diaphoretic and whose lungs are congested is probably having an myocardial infarction. The EKG should reveal changes that are consistent with an injury to the heart. The chest x-ray should show evidence of congestive heart failure. The labs tests are likely to show elevation on the CPK I and troponin, markers for myocardial damage. Recently I examined a pleasant octogenarian. She was in obvious distress. She described her abdominal pain and vomiting. Her distended abdomen was very quiet to auscultation. She had diffuse but only mild tenderness. She had an intestinal obstruction by clinical criteria. The possible causes of any presenting complaint are prioritized by likelihood of death or disability. Vascular causes are usually first on the differential diagnosis list. Does this woman have a leaking aneurysm, or a blocked mesenteric artery? The patient was given medications for pain and nausea and labs where sent off. I also ordered a CT of her abdomen without IV or oral contrast. My radiology colleagues would not be happy but I felt that her kidneys would be damaged by the IV dye and she would not be able to tolerate drinking a liter of oral contrast with a bowel obstruction. Her lab tests where abnormal but not specific. As I looked at the CT images, I was stunned. There are diseases that all doctors learn about but rarely encounter. Gall stone ileus is one of those conditions. The gall bladder is a storage tank for bile. When one eats a meal containing fat, the stomach releases a hormone, cholecystokinin. This messenger travels through the veins of the abdomen and stimulates the muscles in the wall of the gall bladder to contract and send bile down the bile duct to the small intestine. The bile will aid in the digestion and absorption of the fat content of a meal. Bile can become like sludge. Stones of bile salts, cholesterol and calcium salts may form in the gall bladder. Long term irritation of the gall bladder wall by gall stones may lead to a connection (fistula) between the gall bladder and the duodenum, the first section of the small intestine. In this patient, that is what had developed. A 2.8 cm gall stone had passed from the gall bladder directly into the small intestine. It meandered down the intestine until it became stuck. The blockage of the intestine by a gall stone is a gall stone ileus. The CT images were identical to ones I had seen in a radiology textbook many years ago. The patient was transferred to a major academic hospital. I am sure that the young doctors will provide excellent care and have a story to tell when they reminisce about their fascinating cases. Unfortunately the unexpected findings may be bad news for the patient. When I was an attending in a teaching hospital, a resident presented a case of a young woman he had evaluated and was ready to send home. The complaint was of vaginal redness and discharge. The evidence of a yeast infection was obvious on physical exam and KOH prep. I introduced myself to the patient and was shocked by her pallor. She denied any sexual experience, or antibiotic use. I told the patient that we were going to do some blood tests. The resident had made the correct diagnosis of the presenting complaint but had ignored the obvious anemic condition of this unfortunate woman. A CBC came back with severe anemia, and a markedly elevated white blood cell count with evidence of leukemic cells. The oncology service was consulted and the patient was admitted. Her impaired immune system from the leukemia had led to the yeast infection. All ER docs have had the experience of treating a child brought in for a "stomach bug". The persistent vomiting and impending dehydration led the parents to seek help. The child shows clear signs of dehydration but the respiratory rate of 40 fills me with dread. A check of the chemistries reveals a diagnosis of diabetes; treatable but a life altering diagnosis. The practice of emergency medicine is controlled chaos. Being rather compulsive and definitely controlling, I may have been better served in another field of medicine. I considered becoming a pathologist when I was a medical student. My advisor told me: internists knew much and do little; surgeons knew little but did much; pathologists knew all, but too late. His opinion of emergency medicine (this was in the mid 1970's), was that it was not a valid career choice. 34 years later I am still an ER doc.