Case 61
Location: Emergency Room.
Vital signs: Temperature 39,3C(103F); heart rate 112/min, regular; blood pressure 112/70 mmHg; respirations 12 per minute;
HPI:
The patient is a 39-year-old white male who presents with a two-day history of increasing fevers and chills with a temperature up to 39.2 the previous evening. He complains of anorexia, diffuse joint pains, and back pain. He also has some myalgias and has noted several painful spots on his fingers. He denies any chest pain, SOB, palpitations, cough, abdominal pain, headache, and seizures. He is feeling nauseated but no vomiting. His REVIEW OF SYSTEMS is positive for a history of recent IV drug use. His past medical history is significant for personality disorder, tobacco abuse, and alcohol abuse. SH: He smokes 2 PPD for the past IS years, drinks alcohol almost everyday. He admits using IV drug abuse from the past 5 years. He was tested for HIV, and Hepatitis B and C recently for pre-employment and were negative. He is allergic to sulfa. He is not on any medication. How do you approach this case?
1-Order physical exam:
General
HEENT/Neck
Lungs
Heart
Abdomen
Extremities
Skin
Neuro/psych
2-Results:
General: The patient is an ill-appearing white male who appears his stated age. HEENT: Oropharynx is clear, except for some palatal petechiae. Pupils are equal, round and reactive to light. Conjunctivae show a small hemorrhage. Funduscopic examination is unremarkable. Neck: Supple; no lymphadenopathy, thyromegaly or bruits. Cardiovascular: Tachycardic, soft holosystolic murmur heard at the left lower sternal border, increased by inspiration and decreased by expiration. Lungs: Clear to auscultation bilaterally. Abdomen is soft, nontender, nondistended. No hepatosplenomegaly appreciated. Extremities: The other arm shows two recent needle tract marks. There is a fine petechial rash noted of the bilateral lower extremities below mid tibia. Several digits on the feet have splinter hemorrhages. In addition, the digits of the hand show several splinter hemorrhages. There are two palpable painful small violaceous nodules on the digits of the right hand.
Review order:
Pulse oximetry, stat
IV access, stat
CBC with differential, stat
PT/PTT, stat
Blood cultures, stat every 10 minutes x 3
UA, stat
Urine toxicology screen, routine
Chest –X-ray, PA and lateral, stat
ECG, 12 lead, stat
3-Results:
02 saturation is 97% on room air. CBC with differential shows a white count 18,000/cmm with 89% polymorphonuclear leukocytes, 10 band neutrophils, 12 lymphocytes, hemoglobin 12, hematocrit 35.5, and platelets 309,000/cmm. X ray of the chest shows 2 very small wedge shaped infiltrates with cavitation. Electrolytes are normal; BUN is 25 and creatinine is 0.9. PT/PTT are WNL. EKG shows sinus tachycardia. UA is WNL. Tox screen is positive for opiates.
Order:
Vancomycin, IV,continuous
Gentamicin, IV, continuous
Acetaminophen, oral, onetime (for fever)
Normal saline, IV, continuous
*Admit to floor/ward
Vitals every 4 hours
Pulse oximetry every 4 hours
Urine output, routine
Bed rest with bathroom privileges
Pneumatic compression stockings
NPO
*Advance the clock for 8 hours
TEE (Transesophageal echocardiogram), stat
CBC with diff, next morning
Consider ordering following if he was not tested before: HbsAg, routine (For hepatitis B screening)
Hepatitis C antibody, serum, routine
HIV-l/HIV-2 serology, routine
Check “Call me with the next available result”
4-Results:
Preliminary blood culture results show staphylococcus aureus, methicillin sensitive growing in 4 out of 4 bottles. Basic metabolic panel:
Review orders:
D/C Vancomycin (double click on this order; the software will ask you, do you want to cancel this order?)
Order Nafcillin, IV, continuous
Centra line placement, routine (for continued IV antibiotic therapy for a total of four to six weeks).
Daily blood cultures until sterile and once after the completion of antibiotic course (4 to 6 weeks) to document the cure
Examine the patient next day
Interim exam:
The patient’s temperature down trends with a T-max of 37.8 on first day of admission. He is hemodynamically stable.
Order review:
The patient is continued on the nafcillin and gentamicin for five days. He is then switched to nafcillin alone (D/C gentamicin after 5 days).
Smoking cessation
Limit alcohol
Safe sex
Seat belt use
No illegal drug use
Exercise program
Advise patient SBE prophylaxis
* Follow up in 1 week.
Primary diagnosis
Right sided infective endocarditis from MSSA
Discussion:
Early cases of infective endocarditis may be difficult to diagnosis if there is a concomitant infection elsewhere in the body. His physical exam had several findings suspicious for an endocarditis infection including splinter hemorrhages, also nodes on his hands on the pulp of his fingers, petechiae of the lower extremities and on the palate, conjunctival hemorrhages.
‘Duke criteria1 for the diagnosis of IE:
Major:
1. Positive blood cultures
2. Positive echocardiogram for IE
Minor:
1. Predisposing factors such as IV drug abuse
2. Fever of >38C (>100.4F)
3. Evidence of embolic phenomena
4. Evidence of immunologic phenomena such glomerulonephritis, Osier’s nodes etc.
5. Equivocal blood cultures
6. Equivocal echo findings
Presence of 2 major or one major and 3 minor or 5 minor criteria is required for the diagnosis of IE.
What ‘empirical’ antibiotic should I use?
1. In a patient with H/O IV drug abuse, the antibiotic choice should cover MRSA (methicillin resistant staphylococcus aureus) and gram-negative organisms i.e. Vancomycin and gentamicin.
2. Blood culture-negative native valve endocarditis is treated with ceftriaxone and gentamicin.
3. Blood culture-negative prosthetic valve endocarditis is treated with ceftriaxone and gentamicin plus vancomycin.
When should I obtain CVTS (cardiovascular thoracic surgeon) consult?
The indication for cardiac surgery in patients with infective endocarditis is not fully agreed upon. However, some of the indications include, moderate to severe heart failure secondary to valvular dysfunction or partially dehisced unstable prosthetic valve, prosthetic valve endocarditis with Staph aureus or Staph epidermidis or relapse of the prosthetic valve after prosthetic valve endocarditis after appropriate antimicrobial therapy, and large (>10 mm) hypermobile vegetations, which can potentially cause septic embolism.
In patients with suspected infective endocarditis one should aim therapy at the most likely organism. Staph aureus is the most common organism isolated in this setting of IV drug use. The patient should be screened for other signs of endocarditis including a urinalysis which may show hematuria, chest X ray which in this case was suspicious for septic pulmonary emboli which can be seen more often in the setting of tricuspid valve endocarditis in IV drug users. Transesophageal echocardiography has become an important mode of helping to diagnose infective endocarditis and help guide management.
There are a number of complications of infective endocarditis, especially with left sided disease that should be monitored for vigilantly. These are mainly embolic in nature and include CNS embolus with stroke-like syndromes or subtle neurologic defects. Emboli to the kidney may cause focal glomerulonephritis, which induces hematuria, or renal failure may ensure secondary to diffuse proliferative glomerulonephritis. One may see arrhythmias including various degrees of heart block and pericarditis, myocarditis or myocardial abscess. Heart failure as noted above in the indications for surgery is also a potential major complication of infective endocarditis. This patient managed to avoid most of the complications possibly because of early presentation and early treatment of his endocarditis. In patients in whom one suspicious of major complications, it could be appropriate to obtain CT scans of the head, chest, abdomen, and pelvis looking for other sites of embolic disease or infarction. One should monitor as well renal function for evidence of kidney failure secondary to glomerulonephritis or infarction or emboli. The patient should receive four to six weeks total of antimicrobial therapy directed at the results of the blood cultures obtained. In this case with Staph aureus optimal therapy is with the penicillinase resistant penicillin, nafcillin, 2 grams IV Q4H. He also received gentamicin for three to five days initially.
In patients intolerant to nafcillin an appropriate substitute antimicrobial therapy would be cefazolin with or without gentamicin.
In patients who have allergies or who have methicillin resistant Staph aureus, vancomycin would be the agent of choice.
Case 61
Location: Office
Vitals: B.P: 130/76 mm Hg; H.R: 130/min, irregularly irregular pulse; Temp: 38.3C; R.R: 18/min.
HPI: A 60 yr white female who has known H/O CAD, S/P CABG presents to your office with 2-day H/O dizziness, light-headedness, and palpitations. She describes the palpitations as irregular, and almost continuous. She denies any chest pain, angina, SOB, orthopnea, PND, or syncope. She also felt little warm since one day. She denies any cough, URI symptoms, dysuria, abdominal pain, and leg swelling. Her ROS is positive for frequency of urination. PMH: She had undergone 3 vessel CABG 3 years ago after an acute anterior wall MI. Her other medical problems include HTN, Type II DM, hypercholesterolemia, osteoarthritis, COPD, and gout. All: She has no allergies. SH: She quit smoking after her CABG. She occasionally drinks alcohol. She lives with her husband at home. FH: Father died at the age of 70 with MI. Mother died at the age of 68 from stroke. She has one brother and one sister both have HTN, and DM. Meds: She takes ASA 81mg po qd, simvastatin 20 po qhs, lisinopril 5 mg po qd, SL NTG prn, glyburide 5 mg po QD, metformin 850 mg po bid, albuterol puffs prn, and acetaminophen with codeine for osteoarthritis. How do you approach this patient?
1 – Order physical exam:
General
HEENT/Neck
Lungs
Heart
Abdomen
Extremities
Rectal exam with FOBT
2 – Results:
HEENT/Neck is WNL. There are few rales and decreased breath sounds noted at left lower base. Heart exam is WNL. Abdomen is WNL. No edema or JVD noted. Hem negative for stools.
Order review:
Pulse oximetry, stat
IV access
12 lead EKG, stat
3 – Results:
94% on room air
EKG showed atrial fibrillation with rapid ventricular response at a ventricular rate of 120-140/min. There are Q waves in anterior leads,consistent with old MI. LVH pattern is noted.
Order review:
CBC with diff, stat
BMP, stat LFTs, stat
Chest X-ray, PA and lateral, stat
U/A, stat
TSH, stat Free T4, routine
CK MB, and troponin T/I , stat and Q 8hours x 2
PT/INR/aPTT, stat
Treat initially
Cardizem Diltiazem IV, bolus
Order review: TDA IM
A - Activity (Bed rest ? , restricted movements ?, etc)
D – Diet (NPO, Diabetic Diet ? , etc)
M – Medications (Switch to oral if possible)
I – Investigations (Labs) + Input/Output Monitoring + IV Fluids (with frequency)
T – TPR (Temp. Pulse.pressure.Resp.) i.e. Vitals …with frequency
Admit to floor/ward
Telemetry
Vitals Q 4 hours
Pulse oximetry Q4 hours
Order ‘old records’
Diet: Consistent carbohydrate diet
Activity: Bed rest with bathroom privileges
Labs:
HbAlC, stat
Accuchecks QID(4 times a day)
2D-echo, routine
Meds:
Continue all home medications: ASA 81mg po qd, Simvastatin 20 po qhs, lisinopril 5 mg po qd, SL NTG prn, glyburide 5 mg po QD, metformin
850 mg po bid, albuterol prn, and acetaminophen with codeine for osteoarthritis
Start Cardizem (diltiazem), IV drip,
Start Heparin, IV, continuous
PTT every 6 hours
Daily CBC with diff
Call me when lab results available
4 – Results:
CBC with diff showed a WBC count of 12,000 with 3% bands. Hb is 13.S. Platelet count is 230,000. BMP showed a Na: 140, K: 4.0, CL: 102, Co2: 22, BUN: 20, Cr: 1.0. Chest X-ray showed small left pleural effusions unchanged from previous 1 yr X-ray. TSH is l.S. Free T4 is WNL. LFTs are WNL. HbAlC is 7.2. U/A showed positive esterase, 50 WBC, and many bacteria. Urine culture is pending. PT/INR is 14.0/0.98. PTT is 30. First set of cardiac enzymes – negative. 2D -echo showed normal
Order review:
Urine culture and sensitivity
Bactrim
Examine the patient in 2 hours
5 – After 2 hours:
Interim history
Monitor telemetry strip: HR is now 90-100/min; patient is still in atrial fibrillation
Repeat EKG: HR is now 90-100/min; patient is still in atrial fibrillation.
Call me when needed.
Examine the patient in next 6 hours
Again order interim history and monitor telemetry strip
Once the HR is less than 80 D/C Cardizem drip, Start Cardizem PO, continuous
Next day Start Coumadin po continuous Daily PT/INR
Examine next day:
Check CBC, PT/INR, telemetry strip
Once the PT/INR is above 2.0, D/C IV heparin
Discharge the patient
Patient education
Out patient followup in 3 days with repeat CBC, PT/INR
Discussion:
The principle issues in managing a patient with atrial fibrillation with rapid ventricular response include:
1. Rhythm control or rate control
2. Anticoagulation to prevent systemic embolization
3. Correcting the underlying abnormality
Rhythm control: It is indicated in: 1. acute atrial fibrillation (less than 48 hours duration), 2. Hemodynamically unstable patient, 3. patients with acute coronary syndromes, 4. Patients with severe heart failure. It can be done by either DC cardioversion or pharmacologic cardioversion. DC cardioversion is particularly indicated in unstable patients. In stable patients, and patients with a reversible underlying problem can be dealt with either electrical or chemical cardioversion. The commonly used drugs for rhythm control include Class III dofetilide, ibutilide, and to a lesser degree amiodarone. Amiodarone is particularly useful in patients with left ventricular dysfunction. Without chronic antiarrhythmic therapy, only 20-30% of patients who are successfully cardioverted remains in NSR for more than one year. The 2 commonly used medications for the maintenance therapy are amiodarone (patient with left ventricular dysfunction) or sotalol (in patients with CAD).
Rate control: The 3 most commonly used AV nodal blockers for the rate control are beta-blockers, calcium channel blockers, and digoxin. Digoxin is particularly indicated in patients with heart failure or hypotension. In most other situations digoxin is less effective than a beta-blocker or calcium channel blocker. The choice between a CCB or beta-blocker depends upon physician preference, and the patient presentation. Beta-blocker is preferred in patients with H/O angina, acute MI. The use of calcium channel blockers is preferred in patients with chronic lung disease. In most situations Cardizem (diltiazem) is the preferred drug as it is easy to administer in the form of IV drip and the dose can be titrated for a goal heart rate. Patients who fail to respond with pharmacologic treatments require EP study and radiofrequency AV nodal-His bundle ablation.
Choosing between Rate and rhythm control:
Until recently, rhythm control has been the preferred method over rate control for patients presenting with the first few episodes of atrial fibrillation. The thought was controlling the rhythm causes low frequency of embolic events. However, the 2 major clinical trials (AFFIRM, and RACE) have demonstrated no significant difference between the 2 groups in terms of embolic events, functional status, or quality of life. Thus, both rate and rhythm control are acceptable approaches and both require anticoagulation. There is a growing support for rate
Anticoagulation:
There are 3 situations where you should consider anticoagulation: 1. Chronic AF, 2. Recurrent AF, 3. Prior and after cardioversion. AF of more than 48 hours or unknown duration requires at least 3 to 4 weeks of warfarin prior to and after cardioversion. The target INR is 2.5(2.0-3.0). Patients with recurrent or chronic AF should be treated with long-term anticoagulation even if they are in sinus rhythm. Patients who have underlying rheumatic valvular disease, severe LV dysfunction, or recent thromboembolism should receive anticoagulation even if the duration of AF is less than 48 hours.Patients with AF of less than 48 hours duration without concurrent valvular disease, or severe LV dysfunction, or H/O thromboembolism are treated with cardioversion under IV heparin coverage but without long term Coumadin.
The other alternative approach for cardioversion to avoid prior prolonged anticoagulation is TEE guided cardioversion.
When should I admit a patient with AF?
Low risk patients (patients without valvular disease, or severe
Searching for the underlying cause:
The common causes of new onset AF include heart failure, acute coronary syndromes, PE, HTN, hyperthyroidism, and infections. Serum TSH and free T4 should be checked in all patients even if they do not have symptoms of hyperthyroidism as there is a 3 fold increase of AF in patients with subclinical hyperthyroidism (Low TSH and normal free T4). If the AF is caused by an underlying problem, cardioversion should be postponed until the condition has been successfully treated. However, anticoagulation should be started.
Primary Diagnosis Atrial Fibrillation
Case 62
Location: Emergency room
Vital signs: B.P 80/40 mm Hg; P.R: 130/min; R.R: 30/min
C.C: Chest pain from a severe motor vehicle accident (MVA).
HPI:
A 61 year old man involved in a motor vehicle accident (MVA), brought to the ER immediately. He complains of severe chest pain, 10/10, and non radiating. He also C/O shortness of breath. Chest wall impacted the steering wheel. No other history is available. How do you approach this patient?
1 – Order:
IV access
Pulse oxy, stat
Oxygen, inhalation
Order general, lungs, and heart exam
2 – Results:
Patient is in severe chest pain, his extremities are turning blue. Lungs are CTA B/L. There is a 15 cm JVD. S1, S2 muffled. No murmurs heard.
Pulse oxy shows 88% on room air.
Order review:
IV NS bolus, and continue at 150 cc/hr
Elevate the patient legs
Continuous cardiac monitoring
Pericardiocentesis, stat
3 – Results:
Patient started improving
His BP came upto 100/60 mm HG
HR decreased to 90/min
Order review:
ABG, stat
Stat EKG, 12 lead
Chest -X ray, portable
Transthoracic Echocardiogram (TTE), stat
Pericardial fluid for cell count, stat
CVTS (Cardiovascular thoracic surgeon) consult, stat
4 – Results:
12 lead EKG shows sinus tachycardia, low-voltage QRS complexes, and electrical alternans.
CXR showed globular heart with air fluid level in pericardial cavity.
TTE – Revealed fluid in the pericardial cavity.
Impression: Cardiac tamponade
If the CVTS doesn’t want to operate, then the patient management will be as follows:
Shift the patient to ICU
Continue continuous cardiac monitoring
Swan-Ganz catheter, stat
Diet – NPO
Complete bed rest
Pneumatic compressions of the legs
I
Place a Foley catheter
Urine output Q 2 hours
CBC with diff, stat
Basic metabolic panel, stat
PT/aPTT, stat
Type and screen for 2 units of blood
M
Continue NS @ 150 cc/hr
Gastric prophylaxis – Omeprazole (20mg) orally, once daily
Acetaminophen + codeine for pain, continuous (actually as needed in real life)
Note: Transfuse blood if the Hb is less than 8 in a patient with no active bleeding, less than 10 in actively bleeding patient. Each unit of blood will increase the Hb approximately 1 gm%.
5 – Next day:
D/C Foley catheter
Repeat TTE
Repeat Chest -X-ray
Note: If you do this much, your case will end in the exam. Further management is complicated, it is based on the patient condition, CVTS recommendations, etc.
Explanation:
Cardiac tamponade is a life threatening condition and should be diagnosed and treated emergently. The diagnosis of tamponade is primarily clinical. Myocardial rupture in patients with trauma usually manifests itself as cardiac tamponade. The classic description of cardiac tamponade is Beck’s triad: Hypotension (100%), distended neck veins, and muffled heart sounds. The other useful findings are tachycardia, elevated central venous pressure, pulsus paradoxus, and cyanosis of the head, neck, arms, and upper chest. Tamponade should be suspected in any patient with chest injury whose hypotension do not respond to fluids or out of proportion to the apparent blood loss.
Differential diagnosis in patients with trauma should include tension pneumothorax (decreased breath sounds, deviated trachea, hyperresonance to percussion), right ventricle contusion/failure, superior vena cava obstruction, ruptured tricuspid valve, and aortic dissection. Pulmonary embolism, pericarditis, and cardiogenic shock should be considered in patients without trauma.
Emergency pericardiocentesis is a potentially life-saving procedure performed in the ED. Emergent thoracotomy is indicated when the patient does not respond to pericardiocentesis and has rapidly deteriorating vital signs or cardiac arrest. After pericardiocentesis, intrapericardial catheter is left in place and attach it to a closed drainage system. Drain should be checked regularly for reaccumulation of fluid. Pericardial fluid should be sent for cell count initially and periodically (Q 24 hours) to diagnose an impending bacterial catheter infection, which could be catastrophic. If the WBC count rises significantly, the pericardial catheter must be removed immediately. A Swan-Ganz catheter is very useful to monitor the central venous pressure and it can be left in place for continuous monitoring and to assess the effect of reaccumulation of pericardial fluid. Patients should have a repeat echocardiogram and chest x-ray within 24 hours.
Primary Diagnosis:
Pericardial Tamponade
Case 63
Location: Emergency Room
Vitals: BP: 90/60 mm Hg; HR: 124/min; RR: 24/min; Temp: 37.2C (99F) C.C: Sudden onset abdominal pain
HPI:
A 55-year-old white obese female is brought to the ER with abrupt onset of epigastric pain. The pain started 5 hours ago, is steady, boring and severe in nature and radiates to the back. It is made worse by lying supine and is better by sitting and leaning forwards. The patient also has nausea and vomiting. She denies any fevers or bowel or bladder problems. She has a past history of episodic right upper quadrant pain and fatty food indigestion, for which she never sought any medical advice. She has no allergies and is not taking any medications. The patient does not smoke and denies any alcohol use. Family history is non-contributory. Rest of the review of systems is unremarkable.
1 – How would you approach this patient?
The initial approach should be to take some general resuscitative measures, a delay in which might be life threatening. Simultaneously, think of a differential diagnosis and order the relevant tests to rule in and rule out the disease process and its etiology. Remember you always need a thorough physical examination before establishing a diagnosis.
Order No. 1:
IV access, stat
Start IV fluids:
Continuous BP monitoring
Pulse Oximetry, stat
EKG, 12 lead, stat
2 – Results for Order No. 1:
Oxygen Saturation is 95% on room air
EKG shows sinus tachycardia without evidence of ischemia or infarction
Order physical exam:
General apperance HEENT/Neck
Examination of CVS Examination of lungs Examination of Examination of CVS Examination of lungs Examination of Abdomen Examination of Rectum Extremities
3 – Results of Physical Examination:
General appearance: Obese female, ill looking, diaphoretic, restless. HEENT –
Meanwhile the nurse tells you that the pain is worse
Order No. 2:
NPO
Fentanyl or Meperidine, IV, continuous
Phenergan, IV, stat, one time (for nausea)
lab
Serum amylase, stat
Serum lipase, stat
LFTs, stat
Erect abdominal X-ray, portable, stat
CBC with differential, stat
BMP, stat
Calcium, stat
Call me when the lab results available
4 – Results for Order No. 2:
BP – 94/70 mm Hg
Amylase – 500 IU/L; Lipase -160 IU/L
Hgb -13 g/dl, WBC – 14,000/uL, Platelet – 250,000/mm3, leftward shift in differential count
BUN – 30, Creatinine-1.1, Sodium -131 meq/L, Potassium – 3.6 meq/L, Chloride -101 meq/L, Bicarbonate – 26 meq/L, Calcium -10.1 mg %
LFT- Total bilirubin – 6.0 mg %, Direct bilirubin – 4.5 mg %, ALT – 35 IU/L, AST – 40 IU/L, Alkaline phosphatase – 190 IU/L
X-ray abdomen - No air under the diaphragm, no dilated bowel loops
Discussion:
Differential Diagnosis: This is a patient with acute epigastric pain. Your differential diagnosis should include acute gastritis, perforated duodenal ulcer, acute pancreatitis and acute cholecystitis. Important point here is the description of pain that radiates to the back, is made worse by lying supine and is better by sitting and leaning forwards. This is typical of acute pancreatitis and may also be seen with a perforated duodenal ulcer.
Confirming the diagnosis: The diagnosis of acute pancreatitis is confirmed by elevated amylase and lipase with the latter being more specific. These enzymes rise to three times their baseline values within 24 hours in 90 % cases. Besides, you need to order CBC with differential count, BMP, calcium, LFT to look for etiology and assess the severity of the disease that will guide you in the management of the patient. The severity of acute pancreatitis is assessed using the “Ranson’s Criteria” which are not discussed here. A plain X-ray of the abdomen would help in ruling out air under the diaphragm and perforated duodenal ulcer that is high on the list of differential diagnosis.
An ultrasound imaging the liver, gall bladder and biliary tract is a useful initial investigation in patients with suspicion of gallstone pancreatitis and an abnormal LFT. However, ultrasound is a very poor modality for imaging the pancreas. On the other hand, the CT scan of the abdomen can miss gallstones and duct stones but has the advantage of visualizing the pancreas very nicely. It may be ordered when there is a doubt in the diagnosis or when you suspect complications such as necrotizing pancreatitis, pancreatic abscess or pancreatic pseudocyst (discussed in brief later on). Remember, that ultrasound and CT scan of the abdomen are not routinely indicated for establishing the diagnosis of acute pancreatitis but may be useful when indicated; although many may argue for ordering both these tests in most cases of pancreatitis.
Discussion - The above patient results suggest that the patient has acute pancreatitis with hypovolemia and prerenal azotemia.
Likely Etiology: The two most important causes are gallstones and alcohol. The past history of right upper quadrant pain and the LFT results suggest possibility of gallstones pancreatitis in this obese female. Besides, other causes to remember include hypertriglyceridemia (triglycerides>1000 mg %), viral infections (e.g. mumps), drugs (e.g. valproic acid, estrogen, thiazide diuretics, azathioprine, didanosine) and following ERCP. Establishing the etiology is important because unlike other causes where management is conservative, the latest recommendation for gallstone pancreatitis is early ERCP, biliary sphincterotomy and stone extraction. Many a times etiology is not established and is believed to be secondary to “occult biliary microlithiasis.”
Order No. 3:
Transfer to ward or ICU (if unstable or has severe pancreatitis)
Bed rest
Pneumatic compression devises
Urine output
Labs
Ultrasound of liver, gall bladder and biliary tract, stat
Med
Omeprazole, oral, continuous (for stress ulcer prophylaxis)
5 – Results for order No. 3:
BP – 100/70
Ultrasound multinle nalktnnp^ snd dilated nnmmnn hile Hurt
Meanwhile the patient continues to have pain but it is better than before
Order No. 4:
PT/aPTT, stat (preoperative preparation)
Gastroenterology consult for ERCP: Reason: Gallstone pancreatitis; requires possible intervention with ERCP.
Please evaluate and treat.
If the case still continues, order:
Examine the patient 6 hours later
Order, repeat CBC with diff, BMP, Calcium next day.
Management:
In most patients, acute pancreatitis is a mild disease associated with only edema of the pancreatic tissue subsides spontaneously within five to seven days. These patients are managed conservatively.
1. They are kept NPO and put on IV fluids. In severe cases patients may be severely hypovolemic with prerenal azotemia, requiring massive amount of IV fluids for resuscitation. Correction of electrolytes especially hypocalcemia is important.
2. Pain control is achieved using narcotics like morphine, meperidine and fentanyl. Contrary to the previous belief, there is no data to suggest that morphine increases the sphincter of Oddi pressure and may aggravate acute pancreatitis or cholecystitis.
3. Nasogastric suction is reserved for patients with protracted nausea and vomiting or ileus and is not required routinely.
4. If the acute pancreatitis is secondary to gallstones (especially with total bilirubin >S mg % or evidence of acute cholangitis), urgent ERCP and biliary sphincterotomy within 72 hours of presentation can improve outcome by reducing biliary sepsis. If this patient had no gallstones or the LFT was normal then it would be appropriate to manage just conservatively.
5. Acid suppression is necessary only in severely ill patient in ICU settings where the risk of stress ulcer gastrointestinal bleeding is high.
Once the pain subsides, the patient can be started on clear liquids and diet advanced as tolerated.
Complications:
a) Necrotizing Pancreatitis is a more severe form of pancreatitis that usually develops in the second week, requiring CT scan of the abdomen for diagnosis. It is associated with increased mortality and morbidity secondary to multisystem organ involvement including pulmonary (ARDS) and renal (ATN). The necrotic tissue is usually sterile but may get infected. A CT guided aspiration may be needed to confirm infection if patient has persistent fever, leukocytosis, and multisystem organ failure. In addition to the routine measures discussed above these patients require enteral feedings or TPN and antibiotics if infection is present. The antibiotic of choice is Primaxin (imipenem). Further a percutaneous drainage procedure or major surgical debridement may be needed in very sick patients with infected necrotic tissue.
b) Pseudocyst is suspected in presence of severe pain or persistently elevated amylase levels. These are diagnosed with CT scan of the abdomen. Asymptomatic, nonenlarging pseudocysts of less than 6 cm can be followed clinically with serial imaging studies.
Final Diagnosis:
Acute Pancreatitis, secondary to gallstones
Case 64
Location: Office visit
Vitals: BP: 120/80 mmHg; HR: 84/min; RR: 14/min; Temp: 37.2C(99F)
C.C: “I am not feeling well, can’t eat anything and my urine has become dark yellow“
HPI:
A 34-year-old white male photographer comes to the office complaining of ill health for last 1-week. His symptoms began with low-grade fever, generalized body aches and fatigue. He has been nauseated; appetite is poor, with occasional loose stools and vomiting. He has not had any fever for last 2 days but his urine has become dark yellow in color and the stools seem to be very light colored. He also complained of right upper quadrant dull ache. He denied any hematemesis, melena, weight loss or dysuria. There is no history of jaundice or blood transfusion in the past. He has no allergies and is not taking any medications. The patient was a heavy smoker but has developed distaste for cigarettes since his illness started. He denied any alcohol use. He had been to
1 – How would you approach this patient?
A patient with non-specific constitutional symptoms and dark yellow colored urine suggests that this could a patient with jaundice. His vital signs and history suggest that he can be managed as an outpatient and does not need admission. Before ordering any tests, order a complete physical examination to confirm your suspicion. This will also help you in formulating a differential diagnosis and ordering the relevant tests.
Order physical exam:
Complete physical examination
2 – Results of Physical Examination:
General appearance: Well built male, ill looking, not in distress. HEENT: Icteric sclera present; No JVD. Lungs are clear to auscultation and percussion bilaterally; cardiovascular: SI S2 normal, no murmurs, rub or gallop. Abdomen is soft; tenderness is present in the right upper quadrant, but there is no rigidity, rebound or guarding; normal bowel sounds; liver is enlarged about 2 cm below the right costal margin, tender to palpation, firm in consistency with a smooth edge and surface; no splenomegaly or free fluid. Rectal:
Order No. 1:
CBC with differential, stat
Reticulocyte count, stat
BMP, stat
LFTs, stat
PT/INR, stat
*Call me when the lab results available
3 – Results for Order No. 1:
LFT: Total bilirubin – 6.0 mg %, Direct bilirubin – 4.0 mg %, ALT - 980 IU/L, AST – 700 IU/L, Alkaline phosphatase – 190 IU/L, Protein- 7.4 g/dl, albumin-3.8 g/dl. PT= 13.2 sec, CBC: Hgb- IS g/dl, WBC – 9,000/uL, Platelet – 250,000/mm3, normal differential count Peripheral smear: normal; Reticulocyte count: normal
BMP: BUN – 18, Creatinine-1.1, Sodium -138 meq/L, Potassium – 3.8 meq/L, Chloride -105 meq/L, Bicarbonate – 26 meq/L.
Discussion:
The etiology of jaundice can be divided into three broad categories – hemolytic, hepatocellular and obstructive. The hemolytic jaundice is characterized by a triad of anemia, mild jaundice, and splenomegaly but the hyperbilirubinemia is unconjugated (predominantly indirect bilirubin). The peripheral smear may show some abnormal cells suggestive of hemolysis and reticulocyte count is elevated. This patient has jaundice with conjugated hyperbilirubinemia (predominantly direct acting bilirubin) narrowing the possibility to hepatocellular and obstructive pathology. The significant elevation of aminotransferases and only mild elevation of alkaline phosphatase in this patient makes the possibility of obstructive jaundice (e.g. stones, strictures or cancer) less likely. This implies that this patient most likely has a hepatocellular cause. The causes of acute hepatocellular jaundice would include infections (mainly viral), drugs (e.g. acetaminophen), toxins (e.g. mushroom), alcohol and ischemic. Remember that in acute alcoholic hepatitis the AST/ALT ratio is >2:1, but transaminases are never >300.
This patient’s recent visit to Mexico (developing nation), incubation period of 2 weeks after return from Mexico, onset with fever during the anicteric phase, fever resolving with onset of jaundice and aversion to cigarettes suggest viral hepatitis A. Hepatitis A is the most common form of acute viral hepatitis in the USA and worldwide. He does not have risk factors for hepatitis B or C. Remember, that although feco-oral route is the most common mode of hepatitis A infection, homosexual men and IV drug users are also at an increased risk. Its incubation period varies from 15 to 50 days.
Confirming the diagnosis: The diagnosis of acute viral hepatitis can be confirmed by ordering anti-HAV antibodies. These are of two types- IgM and IgG. Both the antibodies may be present in the serum soon after the onset of illness. But the presence of the IgM anti-HAV antibody confirms the diagnosis of hepatitis A. The IgM antibody peaks during first week and disappears within 3-6 months. The presence of IgG anti HAV antibody in the absence of IgM indicates a previous exposure, non-infectivity and immunity against recurring hepatitis A infection.
Order No. 2:
Anti-HAV antibodies (IgM and IgG)
*Could also order a Hepatitis B (HBsAg, IgM anti-HBc ab), Hepatitis C (Hep C antibody) screening panel if risk factors were present,
Rest at home
Antiemetics PRN (Phenergan, oral, continuous because there is no PRN (as needed) option in software)
counsel
Reassure patient
Regular diet
No alcohol
No smoking
Hepatitis precautions counseling
No acetaminophen or hepatotoxic drugs (these are 2 not available in software)
May send the patient home, repeat appointment once the results available
5 – Results for order No. 2:
Patient comes for return visit the next day IgM anti HAV antibody positive IgG anti HAV antibody positive
Order:
Interim history and brief focused physical exam
Results:
Patient feels weak, continues to have poor appetite; vitals stable
Patient questions about prophylaxis for his wife and daughter (May not happen in real exam)
Order No. 3:
May send the patient home again and schedule appointment for 3 days
LFTs in 3 days
PT in 3 days
Notify public health department
* Hepatitis A immune globulin and Hepatitis A Vaccine for wife and daughter (May not happen in real exam)
Results for order No. 3:
Patient comes for a return visit
LFT- Total bilirubin - 8.0 mg %, Direct bilirubin -5.O mg %, ALT – 1500 IU/L, AST – 1300 IU/L, Alkaline phosphatase – 210 IU/L PT/INR- 14.0 sec, INR=1.36
* Patient still feels weak, continues to have poor appetite but vitals stable
If the case still continues, order:
Examine the patient 3 days later Order, repeat LFT and PT/INR in 3 days
Final Diagnosis:
Acute Hepatitis A
Discussion:
Hepatitis A causes a self-limiting acute hepatitis. There are no chronic or carrier forms of hepatitis A. Given the generally benign nature of hepatitis A, most patients can be treated at home with symptomatic and supportive therapies. No specific antiviral treatment is available. Intake of alcohol, acetaminophen and other potentially hepatotoxic substances should be avoided. Remember that conjugated hyperbilirubinemia is seen in viral hepatitis and do not be fooled by light colored stools. These are acholic stools because of cholestatic phase seen in infectious hepatitis causing a picture similar to obstructive jaundice. Do not be scared by high and rising levels of aminotransferases. The aminotransferases may be as high as 5OOO IU/L and may show a rising trend for couple of weeks before starting to resolve. Recovery occurs in 3-16 weeks, although LFT may be impaired till one year. Encephalopathy and coagulopathy point towards hepatic failure and the need for admission.
Does this patient need vaccination?
No, since Hepatitis-A infection leads to life-long immunity.
Case 65
Location: Emergency Room
Vitals: BP: 100/60 mm Hg (supine), 80/50 mm Hg (sitting); HR: 124/min; RR: 24/min; Temp: 98.4F
C.C: Black colored stools
HPI:
A 55-year-old white male is brought to the ER with a history of black colored, sticky, foul smelling stools for 48 hours. He decided to seek medical help after he vomited out bright red blood about an hour ago and felt weak and light headed. He has had six episodes of black stools in the last 24 hours. The patient has had history of epigastric pain for the last 1 month that occurs mostly on an empty stomach and is relieved with food and antacids. He denies history of fissures, hemorrhoids, jaundice or weight loss. He also has chronic low backache for six months. He has no allergies and has been taking over the counter ibuprofen on regular bases. The patient has been smoking one pack of cigarettes per day for the last 30 years. He also drinks beer regularly on weekends and parties. Family history is non-contributory. Rest of the review of systems is unremarkable.
1 – How would you approach this patient?
This is a patient with melena and hematemesis, who is hemodynamically unstable as is obvious from the hypotension, orthostasis and tachycardia. The initial approach should be to take the general resuscitative measures, a delay in which might be life threatening. Simultaneously, think of a differential diagnosis and order the relevant tests to rule in and rule out the disease process and its etiology. Remember you always need a thorough focused physical examination before establishing a diagnosis.
Order No. 1:
Pulse Oximetry, stat
Cardiac monitor, continuous
Continuous BP monitoring
IV access, stat- 2 large (18 G) IV bore needles
Start IV fluids:
Make NPO
2 – Results for Order No. 1:
BP- 100/70 mm Hg; HR- 116/min Oxygen Saturation is 95% on room air
Order focused physical exam:
General appearance HEENT/Neck Examination of CVS Examination of lungs Examination of Abdomen Examination of Rectum Extremities
Results of Physical Examination:
General appearance: Well built, pale looking, anxious male. HEENT: Pale conjunctiva, anicteric sclera, dry mucous membranes; no JVD. Lungs are clear to auscultation and percussion bilaterally. Cardiovascular: Tachycardia, 51 52 normal, no murmurs, rub or gallop. Abdomen is soft, mild tenderness in the epigastric area but there is no rigidity, rebound or guarding; bowel sounds are normal, no organomegaly or free fluid. Rectal:
Order No.2
CBC with differential, stat
BMP, stat
LFTs, stat
Type and crossmatch, stat
PT/INR, stat aPTT, stat
EKG, 12 lead, stat
IV Ranitidine or Pantoprazole (Protonix), continuous (Protonix IV is not available in CCS software)
Discontinue his ibuprofen
NG tube, gastric lavage
3 – Results for Order No. 2:
CBC: Hgb -7.0 g/dl, Hct- 21% WBC – 11,000/uL, Platelet – 250,000/mm3, normal differential count
BMP: BUN – 32, Creatinine-1.1, Sodium -138 meq/L, Potassium – 3.8 meq/L, Chloride -103 meq/L, Bicarbonate – 26 meq/L, Calcium -10.1 mg %
LFT: Total bilirubin – 1.0 mg %, Direct bilirubin – 0.3 mg %, ALT – 30 IU/L, AST – 28 IU/L, Alkaline phosphatase – 100 IU/L
PT=18 sec, INR=1.63 aPTT=38 sec; control=3S sec
EKG shows sinus tachycardia without evidence of ischemia or infarction
Order No. 3:
TDA *Admit in ICU
Continue NPO
Bed rest
Pneumatic compression stockings
Inves, input
Urine output
Meds
Stop IV NS
Start packed RBC transfusion (type PRBC), stat – 3 Units
4 Units fresh frozen plasma (FFP), stat
Hb and Hematocrit every 6 hours (Type H&H)
PT after FFP transfusion
Continue Protonix/Ranitidine infusion
*Call me when the lab results available
4 – Results for Order No. 3:
BP – 110/70 mm; HR- 100/min After 3 Units of PRBC and 4 Units FFP Hgb-10 g/dl; Hct-30% PT=14.5 sec, INR=1.45
Patient feels better
Order No. 3:
Continuous BP monitoring
Continue NPO
Hb and Hct every 6 hours
Gastroenterology consult, routine for EGD (Also order H. Pylor biopsy)
Restart, continuous IV NS
Continue Protonix/Ranitidine infusion
Call me when the lab results available
5 – Results for Order No. 3:
EGD- clean based ulcer in the first part of duodenum. Biopsy taken Hgb-10.2 g/dl; Hct- 30.6 % BP- 120/80; HR- 90/min
Order No. 4
Discontinue NPO
Stop IV NS
Starts clears and advance to regular diet as tolerated
Hb and Hct every 12 hours
Stop IV Protonix/Ranitidine
Start Protonix, oral
5 – Results of order No. 4:
Patient is tolerating regular diet
Hgb-10.0 g/dl; Hct- 30.0 %
BP- 128/80; HR- 74/min
Biopsy is positive for inflammation, ulceration, no malignant cells
Tissue is negative for Helicobacter pylori
Order No.5
Discharge the patient home after overnight watch
Send home on Protonix for 4-8 weeks, Rx helicobacter pylori CAO
Patient counseling
Medication compliance
Start Ferrous sulfate, continuous (Optional)
Avoid NSAIDs (Type – No aspirin)
Stop smoking
Stop alcohol
Recheck Hb and Hematocrit with return visit
Make follow-up appointment in 2 weeks
Discussion:
Differential Diagnosis: Hematemesis and melena suggest upper gastrointestinal (UGI) hemorrhage. UGI bleed by definition is bleeding proximal to the ligament of Treitz. Remember that while presence of hematemesis always suggests UGI bleed, not all patients with UGI bleed have hematemesis. Melena most often is seen with an UGI bleed but may also be seen sometimes with proximal lower GI bleeding. It is in this situation (i.e. melena with no hematemesis) that a nasogastric tube placement and aspiration will be useful. Presence of fresh blood or coffee ground aspirate will suggest fresh or old UGI bleed respectively. The nasogastric tube can then also be used for lavage with tap water to clear the stomach before esophagogastroduodenoscopy (EGD). A negative finding on nasogastric lavage does not rule out an upper GI bleed as bleeding might have stopped or may have been distal to the gastric pylorus. However, a bilious lavage rules out with certainty an upper GI bleed. A nasogastric tube is not needed for diagnostic purposes in this patient, as there was a definite history of hematemesis. However, gastric lavage can be performed for cleaning the stomach.
Hematochezia (bright red bleed per rectum) is seen more commonly with a lower GI bleed but may sometimes be seen with an UGI bleed if it is severe and rapid. The elevated BUN with normal creatinine is another pointer towards UGI bleed.
The most common causes are peptic ulcer disease (stomach or duodenum), gastric erosions and esophageal varices. The less common ones include Mallory Weiss tear (suspect in an alcoholic, with severe retching and vomiting), neoplasm, esophagitis, and arterio-venous malformations. This patient with his history of pain that is relieved with food and use of ibuprofen is certainly a candidate for duodenal ulcer. Other risk factors include smoking and alcohol use.
Final Diagnosis:
Upper gastrointestinal hemorrhage, secondary to duodenal ulcer
Management:
1. Hemodynamic stabilization is more important before an EGD. All patients with UGI bleeding should have two large bore (18 G or larger) peripheral IV lines.
2. Patient should be resuscitated with blood transfusions to keep a hematocrit greater than 30%. If coagulopathy is present, transfusion with FFP and administration of Vitamin K is needed to keep the INR below 1,5, Platelet transfusions may be needed for platelet counts of less than 50,000/ mm3. Calcium levels should be monitored as multiple transfusions may lead to hypocalcemia requiring specific therapy.
3. Once the patient is stabilized the investigation of choice is an EGD that offers diagnostic and therapeutic options. This patient had a duodenal ulcer, which is the most common cause of UGI bleed. The endoscopic appearance of the ulcer predicts the risk of rebleeding and mortality. Since this patient had a clean-based ulcer that carries a very little risk of rebleeding, he could resume a normal diet and be discharged within 24 hrs, as his hemoglobin was stable. Flat spots or adherent clots on EGD need observation on a general floor for 2 to 3 days. Patients with visible vessels or actively bleeding ulcers can be treated with local epinephrine injections. These lesions are associated with the highest risk for rebleeding and such patients need to be monitored in the ICU after the EGD. They should be discharged only after 3 days of stabilization. If during this period of observation rebleeding occurs then a repeat urgent EGD is needed. Such patients might need surgery if recurrent bleeding continues to occur after two endoscopic treatment attempts.
4. IV proton pump inhibitors (PPI) have been shown to reduce recurrent bleeding after endoscopic management of bleeding ulcers and may be continued for 72 hrs after EGD. At the time of discharge the patient should be put on an oral PPI for 4-8 weeks. Repeat EGD on an outpatient basis should be performed in patients with gastric ulcer to ensure healing and exclude underline malignancy. However, repeat EGD is unnecessary in patients with duodenal ulcers.
5. If the biopsy is positive for H. pylori, the patient should receive triple drug therapy for eradication of the organism. NSAIDs, smoking and alcohol need to be stopped to promote healing and prevent recurrence.
6. In patients with known cirrhosis and portal hypertension the most likely source of bleeding is esophagogastric varices. Once these patients are hemodynamically stabilized, octreotide should be started. Besides EGD is performed and sclerotherapy and band ligation of the varices can be done to stop bleeding. If octreotide and EGD intervention do not stop bleeding then a balloon tamponade (for e.g. with a Sengstaken-Blakemore ortube) should be instituted and transjugular intrahepatic portosystemic shunt (TIPS) should be attempted to decrease portal pressure. The TIPS procedure has replaced surgery because of the significantly lower mortality rate. Once the patient has stopped active bleeding he can be discharged on a nonselective beta-blocker (for e.g. nadolol Minnesota
Case 66
Location: Emergency Room
Vitals: BP: 104/70 mm Hg (supine), 80/50 mm Hg (sitting); HR: 120/min; RR: 24/min; Temp: 98.4 (36.9C) C.C: Bright red blood per rectum
HPI:
A 65-year-old white female is brought to the ER with a one-day history of passing bright red blood with bowel movements. She has had three episodes with moderate amount of fresh blood mixed with stools, with no anal pain. Her stools are soft in consistency and there is no history of fissures or hemorrhoids in the past. She felt weak and light headed. There was no history of nausea, vomiting or abdominal pain. She denied any hematemesis, melena, diarrhea, constipation, jaundice or weight loss. Her past medical history is significant for type II diabetes mellitus, hypertension and hyperlipidemia. She has never had a colonoscopy in the past. She has no allergies. Her medications include glyburide, simvastatin and lisinopril. The patient does not smoke or consume alcohol. Her mother died of colon cancer at the age of 60 years. Rest of the review of systems is unremarkable.
1 – How would you approach this patient?
This is a patient with hematochezia, who is hemodynamically unstable as is obvious from the hypotension, orthostasis and tachycardia. The initial approach should be to take the general resuscitative measures, a delay in which might be life threatening. Simultaneously, think of a differential diagnosis and order the relevant tests to rule in and rule out the disease process and its etiology. Remember you always need a thorough focused physical examination before establishing a diagnosis.
Order No. 1:
Pulse oximetry, stat
IV access, stat – 2 large (18 G) IV bore needles
Start IV fluids:
Continuous cardiac monitoring
Continuous BP monitoring
NPO
*If the CCS doesn’t provide orthostatic vitals you can order: Postural vitals, stat
Results for Order No. 1:
BP – 100/70 mm Hg; HR- 124/min
Oxygen Saturation is 97% on oom air
Order physical exam:
General appearance
HEENT/Neck
Examination of CVS
Examination of lungs
Examination of Abdomen
Examination of Rectum
FOBT (not required if u see a fresh bleeding)
Extremities
2 – Results of Physical Examination:
General appearance: Pale looking, anxious female. HEENT: Pale conjunctiva, anicteric sclera, dry mucous membranes; no JVD. No palpable lymph nodes. Lungs are clear to auscultation and percussion bilaterally. Cardiovascular: Tachycardic, SI S2 normal, no murmurs, rub or gallop. Abdomen is soft, non-tender, no rigidity, rebound or guarding; bowel sounds are normal, no organomegaly or free fluid. Rectal:
Order No.2
CBC with differential, stat
BMP, stat
LFTs, stat PT/aPTT, stat
EKG, 12 lead, stat
Type and Crossmatch, stat – in preparation for blood transfusion
Anoscopy, stat
Nasogastric tube, aspiration
Discontinue her glyburide, simvastatin and lisinopril
3 – Results for Order No. 2:
BP – 100/70 mm Hg; HR- 124/min
CBC: Hgb -7.5 g/dl, Hct- 22.5 %, WBC – 12,000/uL, Platelet – 450,000/mm3, normal differential count
BMP: BUN – 25, Creatinine -1.0, Sodium -135 meq/L, Potassium – 3.7 meq/L, Chloride -104 meq/L, Bicarbonate – 25 meq/L
LFT: Total bilirubin – 1.0 mg %, Direct bilirubin – 0.4 mg %, ALT – 31 IU/L, AST – 30 IU/L, Alkaline phosphatase – 110 IU/L
PT=17 sec, INR=1.60; aPTT=39 sec, control=35 sec
EKG shows sinus tachycardia without evidence of ischemia or infarction
Nasogastric aspirate – bilious with no blood
Anoscopy – no anal fissures; no external or internal hemorrhoids; no ulcerations in distal part of rectum
Admit in ICU
Blood transfusion with prolonged PT PTT
Stop IV NS
Start packed RBC transfusion – 3 Units
4 Units fresh frozen plasma (FFP)
H and H every 6 hours
PT after FFP transfusion
TDA
Continuous BP monitoring
Continue NPO
Discontinue NG tube
Complete bed rest
Apply pneumatic compressions for DVT prophylaxis
Input, Inves
Urine output
Accucheck every 6 hours (use regular insulin as needed, based on blood sugar levels)
Examine the patient 6 hours later: order interim history and focused physical exam (make sure you listen lungs as they may develop fluid overload with all the IV infusions).
4 – Results for Order No. 3:
BP - 110/70 mm; HR- 100/min After 3 Units of PRBC and 4 Units FFP Hgb-10.5 g/dl; Hct-30% PT=14.S sec, INR=1.45
Patient feels better; exam looks fine
Order No. 4:
Gastroenterology consult, stat for colonoscopy (Reason: 65 yr old with Hematochezia, no prior Colonoscopy; Please evaluate for the source of bleeding).
Start bowel preparation for colonoscopy – 4 liters of polyethylene glycol (Golytely, Colyte) given over two hours
Vitals every 2 hours
Continue NPO
Restart
H and H every 6 hours
Call me when the lab results available
5 – Results for Order No. 4:
Colonoscopy – Multiple diverticuli in sigmoid and descending colon. Biopsy taken Hgb-10.2 g/dl; Hct- 30.6 % BP – 120/80; HR- 90/min
Order No. 5
Discontinue NPO
Stop IV NS
Start clears and advances to high fiber diet as tolerated
H and H every 12 hours
6 – Results of order No. 5:
Patient is tolerating low roughage diet
Hgb-10.0 g/dl; Hct- 30.0 %
BP – 128/80; HR- 74/min
Biopsy is positive for diverticulosis, no inflammation or ulceration; no malignant cells
Order No.6
Discharge the patient home after overnight watch
High fiber diet
D/C DVT prophylaxis
Restart her home medications
Avoid nuts and fruits with seeds (No option in software)
Follow-up appointment in one week with repeat Hgb and hematocrit.
Discussion:
Differential Diagnosis: LGI bleed by definition is bleeding distal to the ligament of Treitz. Most patients with bright red blood per rectum or hematochezia have a LGI bleed, but about 10% are the result of a brisk UGI bleed. Thus patients with hematochezia should have a nasogastric tube lavage to exclude an upper gastrointestinal hemorrhage. An EGD instead of the usual colonoscopy may be needed to establish the cause of hematochezia in case the nasogastric aspirate shows blood.
The most common causes are diverticulosis, angiodysplasia, polyps and colon cancer in a patient above 65 years. All these conditions are painless, except colon cancer, which sometimes may be associated with abdominal pain. This patient is at a high risk of colon cancer because of a positive family history. Another important cause to consider in this patient is ischemic colitis since she has multiple risk factors for vascular disease. However, ischemic colitis is most often associated with abdominal pain. Also remember, that diverticular bleed usually do not occur in the presence of diverticulitis. Other less common causes include inflammatory bowel disease (ulcerative colitis, Crohn’s disease), vasculitis (Polyarteritis nodosa, Wegner’s granulomatosis), radiation colitis, and infectious colitis (Ecoli, salmonella, CMV).
Management:
1. Hemodynamic stabilization is more important before a colonoscopy. Hemodynamically unstable patients should be admitted in the intensive care unit. Presence of shock, orthostatic hypotension, a 6% drop in hematocrit or blood transfusion requirement of two or more units suggests hemodynamic instability.
2. All patients with GI bleeding should have two large bore (18 G or larger) peripheral IV lines. Patient should be resuscitated with blood transfusions to keep a hematocrit greater than 30%. If coagulopathy is present, transfusion with FFP and administration of Vitamin K is needed to keep the INR below 1,5, Platelet transfusions may be needed for platelet counts of less than 50,000/ mm3.
3. Calcium levels should be monitored as multiple transfusions may lead to hypocalcemia requiring specific therapy.
4. Nasogastric tube lavage should be done. If it shows no blood or has copious bile then the investigation of choice once the patient is stabilized, is colonoscopy. Colonoscopy can localize the site of bleeding, allow tissue biopsies, and therapeutic interventions like injection sclerotherapy and electrocautery. However, a good bowel preparation is needed for good visualization of the colon. If nasogastric aspirate shows blood then an EGD is recommended as the initial investigation of choice. If EGD is negative, then go ahead with colonoscopy.
What if the colonoscopy is normal but the patient continues to have hematochezia?
Order a tagged red blood cell scan (radionuclide imaging study) — Radionuclide scanning is a highly sensitive technique that can detect bleeding occurring at a rate of 0.1 to O.5 mL/minute. However, it cannot localize the site of bleeding and requires presence of active bleeding at the time of the test. If the tagged RBC scan is positive, one must proceed with angiography.
Angiography detects blood loss as low as 0.5 mL/minute. The procedure is 100 percent specific and is performed to accurately localize the site of bleeding, especially if surgical management is needed. It also permits control of bleeding using vasopressin infusion or embolization via the catheter. However, it is an invasive procedure and needs to be performed during active bleeding.
*Remember that angiography is reserved for patients in whom colonoscopy cannot localize the site of bleeding or is not feasible.
When should I get surgery consult?
A surgical consultation is needed for continued severe bleeding with high transfusion requirements. A blind surgery performed without localizing the site of bleeding carries a higher risk of rebleeding. Hence, if feasible a tagged RBC scan and angiography should be done before proceeding for surgery.
Final Diagnosis:
Lower gastrointestinal hemorrhage, secondary to diverticulosis.
Case 67
Location: Emergency Room
Vitals: BP: 80/50 mm Hg; HR: 40/min; RR: 24/min; Temp: 98.4F C.C: Lightheadedness
HPI:
A 55 years old male victim of a motor vehicle accident is brought to the ER by ambulance. He was a unrestrained driver of a car that hit a tree due to poor visibility on that foggy night. The patient complains of mild generalized body ache, severe chest pain and lightheadedness, He remembered his chest having struck against the steering wheel. However, there was no history of head injury, headache or loss of consciousness. He did not complain of respiratory distress. The patient was feeling uncomfortable with the Miami-J collar put by the
1 – How would you approach this patient?
This is a victim of motor vehicle accident, who is hemodynamically unstable as is obvious from the hypotension and bradycardia. The initial approach should be to take the general resuscitative measures, a delay in which might be life threatening. Simultaneously, think of reasons for hypotension and bradycardia in an accident victim and order the relevant tests. Remember you always need a thorough physical examination to rule out serious injuries and decide which body parts to image.
Order No. 1:
Pulse oximetry, stat
IV access, stat-
2 large (18 G) IV bore needles Start
IV fluids:
BP, HR monitoring
Results for order No 1:
BP- 80/50 mm Hg; HR- 34/min Oxygen Saturation is 95% on room air
Order examination:
General
Heart
Lungs
2 – Results of the exam:
General appearance: Well-built, white male, in severe pain, holding on to his chest with his right hand. Lungs are clear to auscultation and percussion bilaterally; Cardiovascular – Bradycardia, variable intensity of SI and S2; no murmurs, rub or gallop.
Order No 2:
EKG, 12 lead, stat
Chest-X ray, PA portable
X-ray cervical spine, stat
IV Fentanyl or Ketorolac, bolus
3 – Results of Order No 2:
EKG shows complete heart block, ventricular escape rhythm with a rate of 40/min, QRS duration of 140 msec. No evidence of ischemia or injury except nonspecific ST/T changes.
Chest X-ray: Fracture of the left 3 and 4 ribs. No pneumothorax or effusion. Heart and mediastinum are normal in size and configuration. X-ray cervical spine:
Order No 3:
Atropine 0.5 mg IV stat
Put patient on transcutaneous pacemaker
Consult Cardiology, stat (for transvenous pacemaker placement)
Consult Orthopedics, stat (to rule out cervical spine injury and get rid of Miami-J collar)
Make NPO
CBC with differential, stat
BMP, stat
PT/aPTT, stat
Results of Order No 3:
CBC: Hgb -13.0 g/dl, Hct – 39% WBC – 9,200/uL, Platelet – 250,000/mm3, normal differential count
BMP: BUN – 19, Creatinine-1.1, Sodium -138 meq/L, Potassium – 3.8 meq/L, Chloride -103 meq/L, and bicarbonate – 26 meq/L.
PT=13 sec, INR=1.23; APTT=33 sec; control=3S sec
Order No 4:
Check the BP and HR
4 – Result of Order No 4:
Transcutaneous pacemaker paces at rate of 80/min, BP-90/60 Patient’s lightheadedness and chest pain is better
Order examination of:
HEENT/Neck
Abdomen
Extremities
Skin
CNS
Results of Physical Examination:
HEENT: Normocephalic, atraumatic, PERLA, EOMI, pink conjunctiva, anicteric sclera, moist mucous membranes, no ear or nose bleed; Neck-Miami J collar on; Abdomen is soft, no tenderness, rigidity, rebound or guarding; bowel sounds are normal, no organomegaly or free fluid. Extremities – no edema, clubbing or cyanosis, no calf tenderness, peripheral pulses feeble. Neurological exam-awake, alert oriented, moves all four limbs with no focal neurological deficits.
Order No. 5:
Continuous HR and BP monitoring
Continue NPO
Continue NS
CK and MB, stat
Troponin T, stat
Echocardiogram, stat
Results for Order No. 5:
CK- 500; MB-11
Troponin T- 0.500
Echocardiogram: EF= 55 – 60, no wall motion abnormalities, all valves are normal, no pericardial effusion
Cardiologist takes the patient to the cardiac cath lab for a temporary transvenous pacemaker insertion.
If case continues further, may need permanent pacemaker insertion.
Discussion:
The most important cause of hypotension in a trauma victim is hemorrhage. The first step in management would be to start IV fluids and send a CBC to look for the amount of blood loss. If there is no overt bleeding one must look for an occult collection in the chest and abdomen, for which you need to do imaging studies. Normally, patients develop tachycardia in response to hypotension secondary to hypovolemia. The bradycardia accompanying the hypotension and the normal hemoglobin in this patient should make you suspicious of an etiology other than bleeding.
The EKG confirms the diagnosis of complete heart block (CHB). CHB is a third degree AV block the diagnosis of which is made by AV dissociation with a slow ventricular escape rhythm of around 40 beats/min. The atria may be in sinus rhythm or in fibrillation but the ‘P’ waves do not bear any relationship with the QRS complexes. However, it is also important to establish the etiology of CHB since it aids in the further management. The most important causes are fibrosis or degeneration of the conduction system and ischemic heart disease. The others include drugs (beta blockers, calcium channel blockers, digitalis, amiodarone), metabolic abnormalities (hyperkalemia), valvular heart disease, and cardiomyopathy (amyloid, sarcoid, hypertrophic cardiomyopathy).
Remember, trauma is an uncommon cause of CHB. Absence of ST-T changes suggestive of ischemia in EKG and no wall motion abnormalities excluded the possibility of acute coronary syndrome. The elevated
The only modality of treatment for complete heart block is pacing. Atropine is only of little benefit and may sometimes transiently improve the heart rate and the blood pressure. These days the life packs are equipped with pads for transcutaneos pacing. But these should be used only as a bridge for the transvenous pacing. The transvenous pacing may be a temporary pacing to begin with. In this patient, if the CHB persists for the next couple of days, a permanent pacemaker can be placed.
Patients with second-degree atrioventricular blocks who are asymptomatic and hemodynamically stable may be managed without a pacemaker. However, a complete heart block even in the absence of symptoms warrants a pacemaker, since you are not sure when the patient may become unstable.
Another important thing is to avoid medications that would cause bradycardia and hypotension. This patient has rib fracture and a lot of chest pain. Use of morphine may worsen his hemodynamic parameters. So, ketorolac or fentanyl would be better options for pain control in these patients.
Final Diagnosis:
Motor vehicle accident with complete heart block (secondary to myocardial contusion)
Case 68
Location: Emergency Room
Vitals: BP: 100/60 mm Hg; HR: 104/min; RR: 30/min; Temp: 100.4F C.C: Generalized bodyache and weakness
HPI:
A 80 years old white male is brought to the ER by his son. His son found him lying in the woods on a hot sunny day. It seemed that the patient had gone for a stroll last evening and fell down. He was unable to get up, shouted for help but could not get any. He had been lying on the ground for the last 24 hours till his son found him. The patient complained of severe bodyache. He felt very weak and was thirsty. He denied having lost consciousness. He did not pass urine for the past 24 hours. There was no history of head injury or seizures. He has no allergies and is not taking any medications. The patient does not smoke and denies any alcohol use. Family history is non-contributory. Rest of the review of systems is unremarkable.
1 – How would you approach this patient?
This is an 80 years old man who had a fall and had been lying on the ground for more than 24 hours on a hot sunny day with no help. He is hemodynamically stable. The generalized bodyache is a hint towards possible muscle injury and should be a guide for ordering further diagnostic tests. Remember you always need a thorough physical examination to rule out serious injuries and decide which body parts to image.
Order No. 1:
IV access, stat
Pulse oximetry, stat
Results for order No 1:
Oxygen Saturation is 95% on room air
Order examination:
Complete examination.
2 – Results of the exam:
General appearance: Well-built, in dirt laden clothes, appears extremely dry and weak. HEENT-normal; Neck- no JVD; Respiratory – Clear to auscultation bilaterally; Cardiovascular- Tachycardia, SI S2 normal, no murmur, rub or gallop; Abdomen-soft, non-distended, non-tender, normal bowel sounds, no organomegaly; Extremities- no edema, clubbing or cyanosis, no calf normal bowel sounds, no organomegaly; Extremities- no edema, clubbing or cyanosis, no calf tenderness, peripheral pulses feeble; Neurological- awake, alert, oriented, no focal neurological deficit
Order No 2:
Start IV fluids:
Insert Foley’s catheter, stat
CBC with differential, stat
BMP, stat
EKG, 12 lead, stat
Urinaria lysis
3 – Results for order No 2:
The nurse reports that the patient could give her only 5 cc of dark brown urine
CBC: Hgb -13.0 g/dl, Hct – 39% WBC – 13,200/uL, Platelet – 250,000/mm3, normal differential count
BMP: BUN - 45mg%, Creatinine-2.6 mg%, Sodium -134 meq/L, Potassium – 5.5 meq/L, Chloride – 92 meq/L, and bicarbonate – 17 meq/L. Calcium- 8.0 mg%
EKG shows sinus tachycardia
Urine dipstick- positive for blood; Urine microscopic- no RBC, no WBC, reddish-gold pigmented casts
Order No 3:
CPK, stat
Ionized calcium, stat
Serum phosphorus, stat
Serum magnesium, stat
Serum uric acid, stat
Urine myoglobin, stat
PT/INR, stat APTT, stat
then
Admit in floor Vitals Q 2 hours
Urine output, hourly
Activity as tolerated
4 – Results of Order No 3:
CPK- 10,500 IU/L
10 cc urine in Urobag
Ionized calcium- 0.99 mmol/L
Serum magnesium- 1.8 meq/L
Serum phosphorus-S.S mg/dl
Serum uric acid- 8.5 mg/dl
Urine myoglobin- positive
PT- 14.2 sec, INR-1.40; APTT-3S sec
Order No 4:
Inform in 4 hours
Result of Order No 4:
BP-110/80 mmHg, HR-104/min Urine output- 75 ml/hr
Order No. 5:
Stop 0.9% Saline
Start 0.45% Saline (with mannitol and Soda bicarbonate added to it)
Titrate the mannitol – bicarbonate drip for urine pH> 6.5 and Urine output of >300 ml_/hr
Monitor urine pH every 1 hour
Check CPK in 4 Hours
Check BMP in 4 Hours
Check Magnesium and phosphorus in 4 Hours
5 – Result of Order No 5:
CPK- 9000 IU/L
BMP: BUN-38mg%, Creatinine-2.1 mg%, Sodium -138 meq/L, Potassium -5.0 meq/L, Chloride -101 meq/L, and bicarbonate – 21 meq/L.
Calcium- 8.2 mg%
Serum Magnesium- 1.4 meq/L
Serum Phosphorus- 5.0 mg/dl
BP-130/80 mm Hg; HR-96/min
Urine pH-7.2
Urine output- 1300 cc in last 4 hours
Nurse says that the patient is feeling better
Order No. 6:
Stop mannitol-bicabonate diuresis
Start 0.45% saline, continuous
Check BMP, every six hours
Check serum magnesium every 6 hours
Check serum phosphorus every 6 hours
Check CPK, every 12 hours
Discussion
This is a case of rhabdomyolysis. Prolonged immobilization and compression of muscles lead to ischemic muscle damage. The hot climate and dehyi contributed to the myoglobin induced acute tubular necrosis. This resulted in acute renal failure with anion gap metabolic acidosis and the electrol abnormalities seen with rhabdomyolysis.
Rhabdomyolysis is a syndrome resulting from skeletal muscle injury with release of myoglobin and creatine phosphokinase (CPK) into the plasma. The myoglobinuria, acid urine pH and renal hypoperfusion resulting from hypovolemia leads to precipitation of heme proteins and acute tubular necrosis.
Etiology:
1. Traumatic causes: Crush syndrome, burns, electrocution,
2. Non-traumatic causes:
f Muscle hyperactivity- strenuous physical exercise, seizures, delirium tremens
f Muscle compression- prolonged immobilization, coma
f Muscle ischemia- acute arterial occlusion
f Malignant hyperthermia, neuroleptic malignant syndrome, hypothermia
f Infections- Viral including HIV, bacterial, etc.
f Drugs – alcohol, heroin, cocaine, amphetamines, zidovudine, statins
f Metabolic disorders- hypocalcaemia, hypokalemia, hypophosphatemia, hypothyroidism, hyperthyroidism, diabetic ketoacidosis
f Metabolic myopathies- e.g. Carnitine palmitoyltransferase deficiency. These should be suspected in patients with recurrent episodes of rhabdomyolysis after exertion.
f Others- carbon monoxide, snake bite
Remember that inflammatory myopathies like polymyositis and dermatomyositis very rarely give rise to rhabdomyolysis and acute renal failure.
Diagnosis:
The most common complaint is muscular pain, which is very non-specific. Moreover, a comatose patient will not complain. Dark brown urine may be the only visible sign. Suspect rhabdomyolysis in a patient with renal failure, who has blood present on urine dipstick but no RBC on microscopic examination. This is because the myoglobin in the urine causes the urine dipstick to be falsely positive for blood. Plasma creatinine concentration rises more rapidly with rhabdomyolysis (up to 2.5 mg/dL per day) than with other causes of acute renal failure. In contrast to other forms of acute tubular necrosis, FENa is less than 1 percent.
The diagnosis of rhabdomyolysis is made by measurement of CPK. It begins to raise 2 to 12 hrs after the injury and reaches its peak value 1 to 3 days after injury. The peak may range from several hundred IU/L to over 200,000 IU/L in a full blown crush syndrome. Therefore, CPK should be measured daily for at least 3 days to follow extent of muscle damage. If the serum CPK remains elevated despite treatment, ongoing muscle injury, necrosis and/or compartment syndrome should be sought.
Myoglobin is also released from the injured muscle. It increases before CPK and decreases more rapidly owing to its clearance by kidneys and metabolism to bilirubin. Therefore, remember that a normal serum myoglobin and absence of myoglobinuria does not exclude the diagnosis of rhabdomyolysis.
Various electrolyte abnormalities result from rhabdomyolysis. These can be better understood by grouping them into two categories
1. Influx from Extracellular compartment into muscle cells- water, sodium, chloride (hypovolemic shock), calcium(hypocalcemia)
2. Efflux from injured muscle cells- potassium(hyperkalemia), purines (hyperuricemia), phosphate (hyperphosphatemia), lactic acid (metabolic acidosis), myoglobin(myoglobinuria, nephrotoxicity), thromboplastin (DIC), creatine kinase, creatinine (increased serum creatinine-to-urea ratio)
Management:
1, Fluid replacement is the mainstay of therapy. Use normal saline and initiate at 1.5 L/hr. The aim is to wash off the myoglobin from therenal tubules, establish a good urine output and prevent or limit acute tubular necrosis. While on one hand many electrolyte abnormalities can precipitate rhabdomyolysis, the syndrome itself can lead to various metabolic derangements. Hence one needs to monitor the BMP and electrolytes very closely for the initial 2 days.
2. Forced alkaline diuresis using mannitol and bicarbonate is recommended by some. Alkalinization of urine prevents precipitation of myoglobin in the tubules. However, this should be used once the BP is stable and a urine output is established using isotonic saline. One has to be careful during such large volume fluid replacement as there is always a risk of fluid overload.
Final Diagnosis:
Rhabdomyolysis due to prolonged immobilization
Case 69
Location: Emergency Room
Vitals: BP: 120/80 mm Hg; HR: 112/min; RR: 28/min; Temp: 37.8C(100F) C.C: Fatigue and right upper quadrant abdominal pain
HPI:
A 74-year-old white male presents to the ER with a 3 days history of fatigue and right upper quadrant abdominal pain. His pain is a dull in character, moderate intensity, poorly localized with no radiation to back or shoulder. It increases with deep inspiration. He denies any fever, cough or sputum production but complains of profuse sweating off and on. He has poor appetite with some nausea but no vomiting. There is no history of bowel or bladder problems. The past medical history is significant for type II diabetes mellitus. He has no allergies and is taking glipizide for his diabetes. The patient denies any tobacco or alcohol abuse. There is no history of sick contacts. He is a widower and lives alone. Family history is non-contributory. Rest of the review of systems is unremarkable.
1 – How would you approach this patient?
This is a 74-year-old patient with acute onset right upper quadrant pain and non-specific constitutional symptoms. First think of a differential diagnosis of right upper quadrant pain. The possibilities are: acute cholecystitis, cholangitis, choledocholithiasis, hepatitis, pyelonephritis, appendicitis, and pneumonia. The absence of dysuria, back pain and normal urine color make the possibility of hepato-biliary and renal pathology a little less likely but not impossible. Moreover, absence of fever, cough and sputum point against the diagnosis of pneumonia. In such a situation one should perform a good physical examination to narrow down the list of differential diagnosis and order relevant tests.
Order No. 1
Pulse Oximetry, stat
Results of Order No.l
Oxygen Saturation- 89 % on room air IV access, stat
Order No. 2
Start oxygen by nasal canula @ 4 L/min
Order physical exam:
General appearance HEENT/Neck Examination of heart Examination of lungs Examination of abdomen Examination of extremities Skin
2 – Results of Physical Examination:
General appearance: Well built male, toxic looking, tachypneic. HEENT: Anicteric sclera, No JVD. Lungs: crackles over the right lung base, no rhonchi or rub; Cardiovascular: Tachycardic, SI and S2 are normal, no murmurs, rub or gallop. Abdomen is soft, non-tender, no rigidity, rebound or guarding; normal bowel sounds; no organomegaly or free fluid. Extremities: No edema, clubbing or cyanosis, no calf tenderness, peripheral pulses palpable. Skin: No rash.
Order No. 3:
X-ray Chest (CXR), PA and lateral, stat
EKG, 12 lead, stat
CBC with differential, stat
BMP, stat
LFT, stat
Lipase, stat
3 – Results for Order No. 3:
X-ray Chest- Right lower lobe infiltrate suggestive of right lower lobe pneumonia, normal cardiac size, no pleural effusion
Hgb -13.5 g/dl, WBC – 16,500/uL, Platelet – 350,000/mm3, Differential count: 90 % polymorphs, 8% lymphocytes, 20 % bands
BUN – 18, Creatinine-1.1, Sodium -138 mEq/L, Potassium – 3.8 mEq/L, Chloride -105 mEq/L, Bicarbonate – 26 mEq/L, Calcium -10.1 mg %
LFTs and Lipase – Completely normal
EKG – Sinus tachycardia
Order No. 4:
TDA
Admit the patient on regular floor
Vitals every 4 hours
Pulse Oximetry, Q 2 hours
Bed rest with bathroom privileges
Pneumatic compression for DVT prophylaxis
Diabetic diet
Diet, oral fluids
Labs
Blood cultures, stat
Sputum Gram stain, stat (Optional)
Sputum cultures, stat (Optional)
Meds
Start antibiotics after drawing blood cultures – Levofloxacin/gatifloxacin or Ceftriaxone + azithromycin, IV continuous
Acetaminophen, continuous (for fever and pain)
Acu checks, QID (4 times a day)
Continue his oral glipizide
Pneumovax and Influenza vaccination if not received earlier
Review after 12 hours
Order interim history and focused physical exam
4 – Results for Order No. 4:
Vitals: BP: 120/80 mm Hg; HR: 96/min; RR: 20/min; Temp: 99 F Oxygen saturation- 100% on 4L/min of oxygen by nasal canula
Order No. 5:
Continue same treatment
CBC/differential after 24 hours
*Call me with the results
Results for Order No. 5:
After 24 hours, the nurse reports that patient feels better.
No nausea; feels stronger and wants to eat
Vitals: BP: 120/80 mm Hg; HR: 80/min; RR: 16/min; Temp: 98 F
Oxygen saturation- 95% on room air
Blood cultures – no growth after 24 hours
Hgb -13.0 g/dl, WBC – 11,500/uL, Platelet – 350,000/mm3, Differential count: 82 % polymorphs, 8% lymphocytes, and 10% bands
Blood sugar – stable on diet and oral hypoglycemics
If case continues- Stop IV antibiotics; plan to send patient home on oral antibiotics for 7-10 days.
Make a follow-up in one week,
Counseling:
Patient counseling Medication compliance
Discussion:
This is a case of community-acquired pneumonia (CAP) with an atypical presentation. With an abnormal chest x-ray, normal LFTs and a benign abdominal examination, no abdominal imaging studies are needed in this patient. Certain important points to remember regarding CAP:
1.Pathogens: The most common pathogens are Streptococcus pneumoniae and Hemophilus influenzae. Staphylococcus aureus, gram-negative bacilli and Moraxella catarrhalis are less common organisms causing CAP. Atypical agents including Legionella, Mycoplasma pneumoniae and Chlamydia pneumoniae although not very common need to be considered when choosing a broad-spectrum antibiotic for empiric treatment of CAP.
2.Clinical Presentation: Cough, sputum production, dyspnea, fevers and sweats are the typical symptoms. However fatigue, headaches, nausea, vomiting, diarrhea and abdominal pain are some of the non-specific and atypical symptoms. Elderly patients (> 75 years) have fewer symptoms of CAP.
3.Diagnostic studies: Chest X-ray is a must for diagnosis of CAP. CBC/Diff, basal metabolic profile, sputum cultures, blood cultures, and pulse oximetry (or ABG) are recommended before starting antibiotics. The role of routine sputum Gram stain and sputum cultures is controversial. These labs may support the diagnosis, identify the pathogen and help in making treatment decisions, regarding the need for admission. Blood cultures are positive in only 11% cases of CAP with Streptococcus pneumoniae accounting for 67% of the positive cultures. In case Legionnaire’s disease is suspected (hyponatremia, immunocompromised, no response to Beta-lactam antibiotics) then urine should be tested for Legionella antigen.
4.Choice of antibiotics:
For a patient being admitted in the general medical floor/ward:
a. Fluoroquinolone alone – levofloxacin or gatifloxacin; Do not use ciprofloxacin
b. 2 /3 generation Cephalosporin (e.g. Ceftriaxone) + Macrolide (e.g. Azithromycin)
“‘Remember, the cephalosporins are not effective against atypicals like legionella, mycoplasma and Chlamydia; hence, it should be combined with a macrolide. Levofloxacin alone also covers atypical organisms.
For uncomplicated pneumonia in the out patient setting: a. Azithromycin or Doxycycline alone
Duration of antibiotics depends upon the pathogen being suspected and treated. In general it varies from 7-10 days. However, it may be 10-14 days for Mycoplasma and Chlamydia and 14-21 days for Legionella.
5.Decision to admit: Various guidelines and scoring systems have been developed to help in deciding whether to admit the patient or not. However, these are difficult to remember offhand. The following major points are poor prognostic factors in patients with CAP. The presence of any of these may necessitate admission.
1. Age greater than 65 years
2. Coexisting disease: Diabetes, renal failure, heart failure, chronic lung disease, chronic alcoholism, immunosuppression, and neoplastic disease.
3. Clinical findings: Hypoxia requiring oxygen; RR >30 breaths/min, Systolic BP<90mm Hg or Diastolic BP< 60 mm Hg,
4. Laboratory tests: WBC <4,000/mm3 or >30,000/mm3; Pao2<60 mmHg; renal failure; multilobar involvement on chest radiograph; pleural effusion; Hct<30%.
Primary Diagnosis: Pneumonia
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