An example write-up is given below to guide the students towards what will be expected for their formal history and physical write-ups. It is also on Blackboard.
The patient is an 80-year-old Japanese gentleman with a history of severe aortic stenosis status post aortic valve replacement, atrial fibrillation with a history of congestive heart failure from diastolic dysfunction, and alcohol abuse with a history of varices who comes in with a chief complaint of, problems breathing and catching my breath associated with swelling of my legs of several weeks duration and more recently intermittent confusion which is related by his son.
History of Present Illness
Mr. T K has difficulty relating his history secondary to a language barrier and mild confusion and his son helps provide historical data for him. I have also reviewed his records at University Hospital. T K has a longstanding history of hypertension and dyslipidemia that lead to severe aortic valve sclerosis and stenosis with subsequent aortic valve replacement in 2004 with a bioprosthetic valve. His valvular heart disease has led to left ventricular enlargement and diastolic dysfunction with a preserved ejection fraction, pulmonary artery hypertension, bi-atrial enlargement and persistent atrial fibrillation. He is not on any anticoagulation which is due to a history of noncompliance. Indeed, he was admitted to the hospital in 2001 with an INR of 9.8. His cardiologist is Dr. RC and I have reviewed his outpatient notes. The anticoagulation for his bioprosthetic valve and atrial fibrillation is management with aspirin only. He has not had any DVTs, pulmonary embolism or strokes. There is no family history of blood clots that he knows of. The last time he was seen by Dr. RC was November, 2008. At that time he was complaining of dypnea and wheezing. He was believed to be suffering from decompensated diastolic heart failure and an echo at that time showed mild concentric left ventricular hypertrophy, the left ventricular ejection fraction was normal, the left atrium was moderately dilated, the right atrium is mild to moderately dilated, and there was mild mitral regurgitation. The gradient across the AVR was 36mmHg. This was unchanged from an echo in 2006. His Lasix was continued and his Atacand was increased. His atrial fibrillation was well controlled at that time.
He does have a significant history of alcohol abuse. He has drunk alcohol for a majority of his lifehe says since the age of 16. He continues to drink alcohol regularly. He says he was in the Japanese Navy, and he was in the military for quite some time. He equates this with a habit of excessive alcohol use. He has drunk large quantities of scotch, whiskey and beer over the years. I could not really quantitate exactly how much over the years he has been drinking, but I get the feeling that he over time has consumed a great deal of alcohol, and, as I mentioned, he continues to drink. I have reviewed his records and he holds no diagnosis of alcoholic liver disease, per se, but has had a remote history of esophageal varices. He knows of no history of liver disease. He denies any history of hepatitis. He has had blood transfusions approximately forty years ago. He denies any history of upper or lower GI bleeding. He did have an upper endoscopy in 2004 prior to his aortic valve replacement that showed only portal hypertensive gastropathy but no esophageal varices.
He appears to have been at his baseline state of health until approximately four weeks ago when he developed shortness of breath and lower extremity edema. At first, the shortness of breath was brought on by exertion and lying flat. It appears to have been only mild and did not change his level of activity or disturb his sleep. Over the four weeks his dypnea has increased to the point that he becomes severely short of breath with ambulating short distances in his home and must frequently stop to rest and catch his breath. He developed orthopnea which has also become progressively worse and about two weeks ago he started to develop disturbances in his sleep. He states he would frequently wake up very short of breath and would sit up on the side of the bed to again, catch his breath. For the last two weeks he has been sleeping in a recliner. He denies and chest pain or pressure. He denies any palpitations. He experiences no nausea or excessive diaphoresis during these episodes. He does not become lightheaded. He does complain of some cough and also some wheezing. No hemoptysis. He has a 50 plus pack year smoking history but is not currently smoking. He has not had any fevers. He really has not had any sputum production. He has no diagnosis of asthma or COPD. He has noticed increasing swelling in his lower extremities. This also started approximately 4 weeks ago with only swelling in his feet, especially the medial aspects of his feet. It became difficult to wear any shoes and he has been wearing sandals or slippers for the last two weeks. The swelling has become progressively worse and now extends up to his waist. He does not weigh himself but all his cloths are much tighter and difficult to put on. He is not very compliant with his diet. He does use a lot of soy sauce and does not appear to make any attempt to modify his salt intake. He has not had any asymmetrical swelling. He has had no trauma to his legs. He has not been bed-bound or hospitalized recently. The legs are painful. He says they ache with an intensity of 3/10 and hurt more at the end of the day or if he has been up walking a lot. They feel better if he puts his feet up. His son states that he has been confused at times over that last week. His son came home to visit around two weeks ago. It appears that Mr. T K drinks a lot more when his son is visiting. About a week ago Mr. T K became progressively more somnolent at times. At these times he also appeared confused. He would be able to answer basic questions but could no longer hold in depth conversations. He had decreased attention. His judgment appeared decreased. He needed help and prompting to do his ADLs and could not do tasks at the level of IADLs. He usually takes care of the household affairs as his wife has Alzheimer's dementia. This was a progressive change and he has not had any focal weakness in any extremities, his son has not noticed any change in his facial symmetry, and he has had episodes of disturb speech but this appears to be associated with alcohol intoxication. No dizziness. No seizures.
His son brought him to the hospital when he realized that Mr. T K could no longer care for his mother and it appears that he needs to travel again for business. He was evaluated in the emergency department and has received Lasix 40mg IV which has improved his shortness of breath slightly. He has been referred for admission to the medicine service.
Past Medical History
- Hypertension. He appears to have had this for at least the last fifteen years. Reviewing his outpatient records his blood pressures average in the upper 140s for systolic pressures and 70s for diastolic pressures, consistent with isolated systolic hypertension. He is on Atacand and Lopressor. His Atacand has recently been changed as mentioned above. His last EKG was in November, 2007 and showed no chamber enlargement by ekg criteria. He does show evidence of hypertensive heart disease on his last echo in November, 2007 with concentric left ventricular hypertrophy. He has not had a microalbumin to creatinine level and his last creatinine was 0.9 in November, 2007.
- Dyslipidemia: Difficult to determine how long Mr. T K has had this. He is not currently treated. A lipid panel in November, 2004 when hospitalized for his valve replacement reveals a HDL of 29 and a LDL of 138.
- Atrial Fibrillation: Diagnosed approximately 10 years ago. He appears to always been easily rate controlled with lopressor. He has been on anticoagulation with coumadin in the past. This was stopped sometime in 2003 secondary to non-compliance. He appears to travel a lot and the patient was not compliant with getting his INR checked. He is asymptomatic. He has never had a syncopal episode or embolic complication.
- Aortic valve sclerosis/stenosis S/P aortic valve replacement: This was diagnosed in 2001 when he started to develop symptoms of dyspnea from congestive heart failure. He underwent cardiac catheterization in 2001, this revealed no significant coronary artery disease, and Normal left ventricular systolic function, Severe aortic stenosis with aortic valve area of 1.40 square centimeters. He refused surgery at that time. He developed worsening congestive heart failure in 2004 and an ECHO revealed a valve area was 0.6 cm squared. A repeat cardiac catheterization revealed no coronary artery disease and he underwent an aortic valve replacement in November 2004 by Dr. P at University hospital. He had a minimally invasive aortic valve replacement with #23 reduced sewing ring, pericardial valve. There were no complications. He is only anticoagulated with aspirin.
- Impaired fasting glucose: Two years ago his primary care doctor, Dr. J M checked fasting blood work that revealed a glucose of 109. There appears to be no repeat. He is treated with diet alone. He has not had a HgA1c or micro-albumin to creatinine ratio. He has no known diabetic retinopathy but has not seen any eye doctor. He has no known neuropathy. He does not check his fingersticks although he does have a glucometer at home.
- Diastolic dysfunction with diastolic congestive heart failure: Diagnosed in 2004 after his aortic valve replacement. Followed by Dr. R C. Last ECHO was Nov. 2007 as mention showing moderate concentric left ventricular hypertrophy with a normal EF. No pulmonary artery pressure was calculated. He has been treated with an ARB, beta-blocker and loop diuretic.
- Hypokalemia: This is secondary to his lasix therapy and he is maintained on potassium replacement therapy daily. No complications noted.
- Low-grade NHL: Diagnosed in May 1996 in response to an abnormal CBC. Diagnosed with stage III non-Hodgkin lymphoma, follicular, mixed. type. He was treated with oral Cytoxan with a fairly significant and dramatic response and long-term remission. He has been followed by Dr. S L at the Regional Oncology Center, last seen May, 2003. Last screening CT was 11/2000. He has remained in remission.
- Alcohol abuse and varices: Mr. T K has a significant history or alcohol abuse. This has also been noted by his primary care physician and oncologist. I can find no study or other objective data of esophageal varices but he has had varices seen at the gastrohepatic ligament and around the porta hepatis region on CT scans of the abdomen done for screen for his NHL. As mentioned a EGD in 2004 showed no esophageal varices but did show portal hypertensive gastropathy. No history of hematemesis or GI bleed. No known history of delirium tremens or alcohol withdrawal and no history of alcohol withdrawal seizures.
No known drug allergies.
- Lopressor 25 mg PO twice a day
- Atacand 16 mg PO daily
- Lasix 40 mg PO daily
- Aspirin 325 mg PO daily
- Potassium chloride 20 mEq PO daily
The patient is of Japanese descent. He moved to the United States in the 1960s. Up until the last two years he would frequently travel to Japan for long periods. This was part of the difficulty in controlling his INR on Coumadin. He was in the Japanese Navy for many years. Mr. T K married. He has been married for over 40 years. His wife has Alzheimer's dementia. Mr. T K has been the primary care giver for his wife over the last few years. He has been able to manage his ADLs and IADLs at least up until the last few months. They live together in a two story home. His son is actively involve in their care but is frequently away. He travels frequently for long periods of time. He does drink alcohol as mentioned above. He appears to have been a moderately heavy abuser of alcohol for approximately 60 plus years. He used to be a smoker. He quit approximately 10 years ago and has an approximately 50 pack year smoking history. He does not use any recreational drugs. He typically eats a traditional Japanese diet and is not restrictive in his salt intake. He has not been very active physically for many years. He has still been able to climb stairs in his house except for the last few days.
His mother died in her eighties from congestive heart failure. The heart failure appears to be a long-standing complication of rheumatic heart disease. His father died at a young age from a trauma. He has a brother that died at the age of 73 from lung cancer. HE has a sister that is still alive. She has severe osteoporosis and arthritis. No other significant family history could be obtained. There appears to be no family history of liver disease.
Review of Systems
Constitutional: No fever, malaise or weakness.
Eyes: No discharge or excessive tearing. No recent changes in vision. Wears glasses for reading only. Has had episodes of blurry vision in the past. Has not seen an eye doctor in many years. No diplopia. No known history of cataracts or glaucoma.
Ears Nose Mouth Throat: Patient is hard of hearing, left greater than right. Has never been tested. No earaches or infections recently. No discharge. No tinnitus or vertigo. No nosebleeds recently, he did have nosebleeds in past associated with high INR values, no sinus pain, no nasal discharge or drainage. Wears upper and lower dentures. Dentures obtained many years ago in Japan. They dont fit very well. No sores associated with dentures. Positive hoarseness of voice and sore throat in the early mornings frequently.
Cardio-vascular: As mentioned in HPI.
Respiratory: As mentioned in HPI.
Gastrointestinal: No nausea, vomiting, or diarrhea. No constipation. No melena or hematochezia. He has had hematochezia in the past associated with hemorrhoids. No dysphagia or odynophagia. No abdominal pain. Positive for heartburn intermittently. No changes on bowel habits or stool. No history of jaundice.
Genitourinary: No history hernias, no testicular pain. Positive scrotal swelling as mentioned but no history of epididymitis or prostatitis. Uncircumcised with no history of complications. Positive history of nocturia approximately 3 times per night. Positive polyuria, hesitancy and post void dribbling and intermittency. Positive weak stream. No dysuria. No UTIs. NO incontinence.
Integument: New mild erythema of the lower extremities, mild puritis associated. Long standing discoloration or lower extremities below the knees. Some benign moles that are followed by his primary care doctor.
Musculoskeletal: No myalgias. Positive arthralgias in his knees bilaterally worse on the left. Worse with ambulation and prolonged standing. No history of gout. No significant joint stiffness. No red swollen joints.
Neurological: As mentioned in HPI.
Psychiatric: No recent depressive symptoms. No anxiety. No changes in mood. No history of mental illness.
Endocrine: No heat or cold intolerance, excessive sweating. No history of thyroid problems or goiter. No polydipsia or polyphagia.
Hematology/Lymphatic: No history of anemia, frequent infections or excessive bleeding. No easy bruising.
Vitals: At the time of my examination, the patient is afebrile with temperature of 36.3 degrees Celsius. His blood pressure is 104/50. His heart rate is 78. His respiratory rate is 24. His pain is rated at 2/10 located in his lower extremities. His O2 saturations are 96% on 3 liters nasal cannula. His weight is recorded at 240 pounds. Since the lasix in the ED he has put out about over a liter of urine.
General: The patient is an obese Japanese gentleman lying in bed at about a 30-45-degree angle in no acute distress and mildly dyspneic. He does have some audible expiratory wheezes. He does not have any cough. He appears disheveled and mildly somnolent. His son and wife are at his bedside.
Eyes: His sclera are anicteric but mildly injected. He does have arcus senilis bilaterally. Fundiscopic exam reveals no papilledema or obvious neovascularization, hemorrhages, or exudates. No AV nicking could be seen but he does have copperwire changes. He does have peri-orbital edema. There are no other significant abnormalities.
ENMT: His oropharynx reveals a class IV oropharynx. He has poor dentition. He wears dentures on top and bottom. Otherwise he is essentially edentulous. The oropharynx is free of any erythema or exudates. His membranes are moist. Otoscopic exam reveals mild cerumen in the left ear and moderate in the right. Both tympanic membranes are pearly gray with mild white scaring. No sign of infection. Nares are patent bilaterally with no evidence of inflammation or discharge.
Head and Neck: He is normocephalic and atraumatic. His neck is very thick due to obesity. His thyroid is symmetrical without enlargement or nodules. The trachea is midline.
Cardiovascular: His heart rate is regular. He has an irregularly irregular rhythm consistent with atrial fibrillation. However, it is not particularly that irregular and certainly very well rate controlled. Heart sounds are distant. He does have a muffled S1. He has a grade 2/6 systolic murmur heard best at the aortic area. It radiates to the carotids. He has no diastolic murmur. I cannot hear any gallop rhythm. S2 is crisp. He has no carotid bruits. His PMI is shifted leftward and is enlarged. He does have anasarca. He has moderate pitting sacral edema. He has moderate body wall edema. He has got extensive and severe pitting edema of his lower extremities. It is symmetrical. His neck veins are distended. Even at about almost upright, I could not see the meniscus of his JVD, although his obesity may be limiting this, but his neck veins are certainly distended, and he has an elevated JVD. He also has hepato-jugular reflux. He does have good pulses in the radials bilaterally and barely palpable pulses in the dorsalis pedis bilaterally limited by the pitting edema. His extremities are warm with good capillary refill.
Pulmonary: His respirations are tachypneic. He is not using any accessory muscles. He does become more short of breath and tachypneic when placed in the supine position. He does have an audible expiratory wheeze with and without the aid of the stethoscope with a prolonged expiratory phase. On inspiration he has vesicular breath sounds with decreased breath sounds at the bases, right greater than left with inspiratory rales above this bilaterally. There are no rales at the mid and upper lung fields. The bases are dull to percussion and display decreased fremitus bilaterally right greater than left. There is no signs of consolidation. He is moving air moderately well.
GI: The exam is limited due to his obesity and body wall edema, but he has positive bowel sounds. His abdomen is soft. It is moderately obese. It is dull to percussion laterally. There is shifting dullness. I could not appreciate a fluid wave. He is tender is the right upper quadrant and his liver is enlarged and palpable below the costal margin. It appears to be consistent with tender hepatomegaly. The remainder of the abdomen is nontender and I could not palpate any mass and there is no rebound tenderness, guarding or rigidity. Rectal exam reveals mild external hemorrhoids and brown stool. The prostate is enlarged, smooth, symmetrical and non-tender.
Chest: He does have a post thoracotomy scar that is well healed. He does have mild gynecomastia bilaterally, The breasts are non-tender.
Skin: He does have stasis-dermatitis-type changes in his lower extremities. The lower extremities reveal a dark bluish-brown discoloration of the lower aspects of the legs mostly to the medial and anterior aspects. The skin is also thickening. Dry and mildly scaling. His legs are diffusely mildly erythematous at the sites of the swelling. He has a few spider angiomas on his upper chest and has bilateral palmer erythema and Terry nails. He also has some telangectasias on his cheeks and nose.
GU: He has an uncircumcised penis. The foreskin retracts easily and there are no signs of infection or discharge under the foreskin. He has a foley catheter in place. He does have mild to moderate scrotal edema. The scrotum is tender to the touch. There are no signs of skin breakdown or cellulitis.
Musculoskeletal: He has fair muscle tone and bulk in the muscle groups of the upper and lower extremities although the edema of the lower extremities limits this exam. The muscles are non-tender to palpation. I do not appreciate any significant soft tissue swelling other than the diffuse edema. There are no red, swollen, warm joints. He as limited range of motion at the knees, hips and ankles bilaterally secondary to the edema. No crepitus or pain on range of motion. He has full range of motion at the shoulder, elbows and wrists. The neck is soft and supple. No tenderness down the spine. His knees reveal bony hypertrophy and arthritis bilaterally.
Lymphatic: I cannot appreciate any cervical, supraclavicular, axillary or inguinal lymphadenopathy.
Neurologic: Cranial Nerves: I- Not tested, II- Vision intact bilaterally using snellen chart, no visual field defects by confrontation. III, IV, VI- Extra-ocular movements intact, pupils equally round and reactive to light. No lid lag. V Sensation intact at forehead, cheeks and jaw bilaterally, jaw strength intact. with clenched teeth. VII- facial features symmetrical with wrinkled forehead and smile. VIII- Patient cannot hear whispered voice in left ear but can in right ear. Weber test lateralizes to the right and air conduction is heard longer than bone conduction on the left. IX Gag reflex intact and swallowing intact. X Palate and uvula symmetrical. XI Shoulder shrug symmetrically intact XII- tongue midline with protrusion.
Strength: Strength 5/5 bilaterally to resistance to the deltoids, biceps, triceps, wrist extensors and flexors and with hand grip. Strength 4/5 bilaterally to resistance to the iliopsoas, 5/5 to resistance to the quadriceps, hamstrings and with dorsi-flexion and plantar-flexion of the ankle and dorsi-flexion of the great toe.
Deep tendon reflexes: 2+ responses to the biceps and triceps reflex bilaterally. 2+ responses to the patellar and ankle reflex bilaterally. Plantar responses are down going bilaterally.
Sensation: Sensation is intact to light touch at the upper extremities bilaterally. Sensation is intact to light touch at the thighs bilaterally but the patient has decreased sensation to light touch below the knees. Particularly at the feet. He responds to painful stimuli at the feet bilaterally.
Cerebellar function: Patient performed well with finger-to-nose testing bilaterally and had difficulty with heel-to-shin testing bilaterally secondary to edema.
Gait and balance: Not assessed.
Psych: He is awake, and slightly lethargic but is easily arousable to an alert status. He is oriented to person, month and year although he could not tell me the exact date. He knows he is in the hospital but does not know which one. He appears to have limited insight and judgment into his medical problems.
Sodium 130, potassium 4.2, chloride is 104, bicarbonate is 34 up from 29 at admission, calcium is 9.4, magnesium 1.5, phosphorus 4.1, BUN is 12, creatinine is 0.9, and glucose is 120. He has had 2 sets of CIPs. Both of them are completely normal. His proBNP at admission was 844. His white blood cell count is 4.8 with a hemoglobin and hematocrit of 11.1 and 32.6 and a platelet count of 102. His mean cell volume is 109. His differential is benign. His urinalysis shows a trace of mild leukocyte esterase and 22 white blood cells per high-power field and 1+ bacteria. There is 30 mg/dl of protein. Otherwise, the specific gravity is 1.005.
Chest x-ray: Was personally reviewed and shows bilateral effusions, greater on the right, and bibasilar opacities which is likely atelectasis, He does have cardiomegaly, and he has bilateral hilar prominence with increased interstitial markings.
EKG: The EKG shows atrial fibrillation at a rate of 75 beats per minute. He has a normal intraventricular conduction. He has a QTc at 458 msec. Axis is normal around 70. He does not have any Q waves. He has low-voltage QRS as he does have poor R-wave progression on the precordial leads. I do not appreciate any significant ST deviation. He has a lot of nonspecific T-wave abnormalities. Compared with a previous EKG, I really do not appreciate any significant changes.
Mr. T K is an 80-year-old male with hypertension, dyslipidemia, a history of aortic stenosis status post valve replacement with a bioprostethic valve, impaired fasting glucose and obesity. He has a long standing history of diastolic congestive heart failure and atrial fibrillation. He has a long standing history of alcohol abuse and known varices. He presents with progressive dyspnea and orthopnea and wheezing associated with progressive lower extremity edema and recent mental status changes. On exam he is hypotensive, tachypneic and hypoxic with decreased breath sounds at the bases with rales. He has a positive JVD and hepato-jugular reflux. He is anasarcic. He has stigmata of chronic liver disease and venous stasis. His labs reveal hyponatremia, macrocyctic anemia and thrombocytopenia. He has pyuria. His chest x-ray reveals effusions and interstitial infiltrates. His ekg is unchanged and shows atrial fibrillation.
- Decompensated diastolic congestive heart failure
- Altered mental status
- Impaired fasting glucose
- Elevated Bicarcarbonate
- Benign prostatic hypertrophy/Bladder outlet obstruction
- Atrial fibrillation
- Aortic valve replacement
- Venous insufficiency
- Gastroesophageal reflux disease
- Alcohol abuse
- DVT prophylaxis
Assessment and Plan
Decompensated diastolic congestive heart failure/dyspnea/hypoxia: The patient appears to have decompensated in regards to his known diastolic heart disease. His hemodynamic profile appears to be wet and warm suggesting only backward failure. Although his blood pressure is soft I feel this is likely due to his liver disease and given his kidney function and warm extremities he appears to be perfusing well. I dont think his mental status changes are from hypo-perfusion. He shows evidence of left-sided failure with mild pulmonary congestion and pleural effusions and right-sided failure with elevated JVD, hepatojugular reflux and peripheral edema. I do not think the degree of anasarca displayed can all be attributed to his congestive heart failure though. This is likely due to his comorbid liver disease. His diastolic heart failure appears to be secondary to long standing hypertension and his history of aortic stenosis. He has had two negative cardiac catheterization but I cannot rule out new onset ischemia as a cause of his decompensation. With his muffled heart sounds, low voltage QRS complexes on EKG and anasarca I also cannot rule out a pericardial effusion either. The dyspnea and orthopnea are caused by the effusions and mild pulmonary congestion. The lack of acute pulmonary edema is likely due to the long standing progressive nature of his diastolic dysfunction with resultant pulmonary artery hypertension and progressive compensation. This likely also explains the only mild elevation in his BNP. The wheeze may be a cardiac wheeze from the pulmonary edema but I cannot rule out other bronchoconstrictive disease. The ascites and obesity is also likely adding a degree of restrictive physiology to his breathing adding to his shortness of breath and hypoxia. He appears to possibly be retaining carbon dioxide with his elevated bicarbonate level but without an ABG I will not be able to determine his acid base status and if indeed he has acute or chronic respiratory acidosis or both. He has a low pretest probability of a DVT and PE and I dont think a PE is playing any part in his dyspnea and hypoxia. The above explanation is much more likely.
I would like to admit the patient to a telemetry bed and begin a lasix drip at 5mg/hr to ensure a slow and progressive diuresis and avoid worsening his hypotension. I will place a foley for accurate monitoring and patient comfort. I will want daily weights and I/O monitoring Qshift to manage his fluid balance. We will follow his electrolytes and kidney function daily with daily BMPs. Replace his electrolytes daily but will also add potassium chloride 40 meq daily in anticipation of hypokalemia from the diuresis. I will obtain an echocardiogram to assess the structure and function of his heart, the integrity of his bioprostetic valve and for any pericardial effusions. I will specifically also ask for assessment of his pulmonary artery pressures. I will rule him out for ischemia with three sets of CIPs. He may eventually need a stress test but not until he is more compensated. I will obtain an ABG to assess his acid-base status and determine if he is retaining carbon dioxide. I will continue the lopressor at 25mg BID and the Atacand at 16mg daily. I will place him on oxygen with 2 liters nasal cannula to keep saturations greater than 92%.
Cirrhosis: Given the stigmata of chronic liver disease on examination and his long standing history of alcohol abuse and apparent sign of portal hypertension it appears that Mr. T K most likely has cirrhosis from alcohol abuse. The hyponatremia, macrocytic anemia and thrombocytopenia also fit into this clinically. He has risk factors for hepatitis and this indeed may be comorbid. He may also have fatty liver from his obesity and metabolic disease. Cardiac cirrhosis from long standing right-sided failure is unlikely given his normal right ventricular function and structure on previous echocardiograms. The anasarca may also be a manifestation of his liver disease with likely low albumin and sodium and water retention. He may benefit from spironolactone. The hypotension is also likely from the liver disease with low albumin and splantic vaso-dilation.
I will check a hepatic and coagulation panel to assess the metabolic and synthetic function of the liver and to assess for any hepatocellular injury or infiltrative process. I will check hepatitis serologies and an iron profile. I will order an ultrasound of the abdomen with doppler to assess the structure of the liver, to assess portal flow and rule out budd-chiari syndrome and portal vein thrombosis. I will also ask to assess for splenomegaly and any liver masses to assess for hepatocellular carcinoma. I will also check an AFP level. If the patient does turn out to have decompensated liver disease I will add spironolactone 25mg orally daily and titrate this up. This will be added to the outpatient regimen with lasix in a spironolactone to lasix ratio of 100:40. This should also help with the hypokalemia.
Altered mental status: This appears to be intermittent and mild. I do not feel that this is secondary to a dementing illness. An acute delirium from his UTI, decompensated heart disease or another process is possible. Certainly with the possibility of liver disease hepatic encephalopathy will need to be considered at the top of the differential. He has no focal neurological deficits and a CT scan of the head will likely not reveal any abnormalities, except with his cardiac history and the fact that he is not sufficiently anticoagulated with an AVR and atrial fibrillation I cannot rule out a stroke.
I will start the work-up with a CT scan of his head without contrast. I will obtain an ammonia level. If elevated, I will start lactulose 30ml every six hours orally titrated to 3 or more bowel movements per day and assess him for any precipitating factors. I will try to limit intervention that may exacerbate a delirious state. I will order a toxicology screen. Once an acute process is corrected or ruled out he will need a full mental status examination.
Ascites: This is most likely portal hypertensive related given the finding consistent with portal hypertension on EGD and CT scan of the abdomen. Most likely related to cirrhosis but cardiac ascites from acute right-sided heart failure is also a possibility. New onset ascites is an indication for paracentesis. I doubt the patient has SBP as even though the patient has mental status changes there is no abdominal pain, fever or leukocytosis.
I will start by assessing the degree of ascites on ultrasound of the abdomen and begin treating with sodium restriction and diuresis with a lasix drip. As mentioned above I may start a regimen of spironolactone and lasix for his probable cirrhosis. I will assess him daily for SBP. For now I am going to hold off on paracentesis.
Bronchocontriction: The patient has a long smoking history and certainly may have COPD. If he does he appears to fit in with the picture of chronic bronchitis rather than emphysema. It is difficult to assess, at this time, whether he meets the diagnostic criteria of cough and sputum production greater than 3 months per year for two or more years. The patient has never had pulmonary function tests. He will need to be at his baseline in regards to his volume status and his congestive heart failure before pulmonary function tests will be useful. Patient with chronic bronchitis tend to retain carbon dioxide. His bicarbonate level is elevated. As mentioned I will need an ABG to assess his acid-base status.
I will start bronchodilators with xopenex 1.25mg nebulized every 8 hours. I will use Xopenex over albuterol to decrease the possibility of worsening his atrial fibrillation. I will also give his atrovent 0.5mg nebulized every 8 hours. I will provide him with xopenex 1.25mg nebulized every 2 hours as needed for wheezing. I will hold off on any steroids inhaled or systemic at this time. I will diurese the patient as mentioned above and follow his pulmonary status daily and with oxygen saturations every shift. I will place him on oxygen at 2 liters nasal cannula to keep his saturations greater than 92%
Obesity: This has been a long standing problem. Due to the history of non-compliance and his inability to exercise this will be very difficult if not impossible to modify. He may certainly have restrictive lung disease from his obesity and lung volumes with his pulmonary functions tests would help assess this. He may also have sleep apnea and obesity hypoventilation syndrome. He will need to take a history specifically for this problem. We can screen him here in the hospital with an overnight oximetry. He will then need a formal sleep study. I question his compliance with CPAP if indeed he is diagnosed with this disorder. This may also add to the possibility of pulmonary hypertension.
I will council him on his obesity and his need to lose weight. I will also screen him for obstructive sleep apnea once his volume status and congestive heart failure is better controlled as this may lead to false positive results.
Pyuria: His pyuria is of questionable significance. He has symptoms of bladder outlet obstruction and may be retaining urine. This will increase his risk for a UTI. Other than the polyuria he has no other symptoms suggestive of a UTI.
I will wait for the culture to return from this urine sample. If indeed a pathogen is found I Will treat as indicated. If not I will repeat the urinalysis for resolution of the pyuria.
Benign prostatic hypertrophy/Bladder outlet obstruction: He appears to have BPH. He will need a PSA level as an outpatient. I would not check a level now since the patient has had a prostate exam and foley placement, both of which will cause elevation of the PSA acutely.
For now I will place a foley to insure adequate drainage. The ultrasound of the abdomen will assess for any hydronephrosis indicating obstruction. I will start the patient on finasteride.
Atrial fibrillation: This appears to be well rate controlled at this time. This is certainly not helping his congestive heart failure. He has many risk factors requiring anticoagulation with Coumadin including valvular atrial fibrillation, hypertension, diabetes, congestive heart failure and age greater than 65. I agree, however, with not using coumadin on this patient due to his non-compliance. He appears to be doing well with just aspirin.
For now I will continue rate control with lopressor 25mg orally BID and anticoagulation with aspirin. I will place him on telemetry.
Aortic valve replacement: This appears to be stable. The cardiac exam reveals no diastolic murmur.
I will assess the integrity of the valve with an echo and continue the aspirin therapy with aspirin 325 mg orally daily
Venous insufficiency: He appears to have bilateral lower extremity venous insufficiency that has started to cause chronic changes and stasis dermatitis. He is at risk for ulceration and chronic venous insufficiency wounds.
I will try to decrease the degree of edema with diuresis. He should have the legs elevated as much as tolerated to aid in drainage. Once the edema has decreased significantly he should wear compression stockings to slow the progression of the soft tissue damage from the edema.
Gastroesophageal reflux disease: Given his symptoms of heartburn and early morning hoarseness and sore throat it appears the patient is suffering from GERD. This is likely worse lately with the ascites and increased obesity.
I will start the patient in the hospital on protonix 40 orally daily. This will also provide the patient with GI prophylaxis.
Alcohol abuse: The patient needs to quit drinking alcohol to slow the progression of his probable cirrhosis.
I will council the patient on the abuse of alcohol. I will also follow the patient closely for signs of alcohol withdrawal. If indeed he starts to withdrawal I will place him on a CIWA protocol with standing and PRN ativan.
Hypertension: The patient is actually mildly hypotensive at this time. He is however asymptomatic. He requires the lopressor and Atacand for his atrial fibrillation and congestive heart failure respectfully.
For now I will continue the lopressor and Atacand as mentioned above. I will hold the Atacand if his pressure drops below 100 systolic or he becomes symptomatic.
Impaired fasting glucose: The patient Likely still has impaired fasting glucose if he has not progressed to diabetes. He has not been eating much for the last few days and his glucose is likely not to poorly controlled.
The patient will be NPO for now and I will place him on a Regular insulin sliding scale every six hours to cover him with 2 units of regular for a glucose level greater than 150 and increasing by 2 units for every 50 mg/dl increment above this. I will check a HgA1c.
Dyslipidemia: He is not on any therapy at this time. I have no recent values.
I will not check lipids during this hospitalization and I will leave this up to his cardiologist once discharged.
Anemia: Likely secondary to marrow suppression for the alcohol abuse given the macrocytosis. I cannot rule out vitamin B12 or folate deficiency. He could also have a myelodysplastic disorder. I doubt that he has had a return of his NHL.
I will check a vitamin B12 and folate level. I will guaic his stools to insure that he has no occult blood. I will review a peripheral smear.
Thrombocytopenia: Likely due to sequestration for splenomegaly from his portal hypertension and from decreased thrombopoetin production from the cirrhotic liver.
I will follow his platelet count. I will assess for splenomegaly by ultrasound.
DVT prophylaxis: I will start heparin 5000 units subQ every eight hours.