Intern Report 7.6

Case Presentation by Dr. Megan Wolf, MD

HPI:
An 86-year-old female presents with 3 weeks of gradually worsening diffuse dull constant abdominal pain.  Her abdominal pain is exacerbated by movement and is not relieved by any particular factors.  It does not radiate anywhere. She has also had decreased appetite and multiple episodes of nonbloody emesis. She has not had a bowel movement in 3 days.

REVIEW OF SYSTEMS:
Constitutional: Denies fevers or chills. Reports weight loss.
Cardiovascular: Denies chest pain.
Respiratory: Reports shortness of breath.
Gastrointestinal: Denies diarrhea or blood in the stool.

PAST MEDICAL HISTORY: hypertension, diabetes, cholelithiasis

PAST SURGICAL HISTORY: cholecystectomy

MEDICATIONS: None

ALLERGIES: No known drug allergies

SOCIAL HISTORY: Denies alcohol, tobacco, and drug use.

PHYSICAL EXAM:
Vitals: BP 94/53, HR 87, RR 24, T 36.2, SpO2 100% on room air
General: Overweight elderly female who appears uncomfortable.
Head:  Atraumatic, normocephalic.
Eyes:  No conjunctival pallor. No scleral icterus.  Pupils equal, round and reactive to light.  Extraocular movements intact.
Nose, Mouth, Throat: Moist mucous membranes.  Uvula midline.
Neck:  Trachea midline.  No jugular venous distension.
Respiratory: Tachypneic. Clear breath sounds bilaterally.  No rales, wheezing, or rhonchi.
Cardiovascular:  Regular rate and rhythm with no murmurs, rubs, or gallops.
Gastrointestinal:  Abdomen is markedly distended and tense. Significant dullness to percussion.  A fluid wave is noted. Tenderness to palpation diffusely throughout the entire abdomen.  Bowel sounds are present.  No organomegaly.
Extremities: 2+ pulses in all extremities.  No lower extremity edema.
Skin: Warm and well perfused. No rashes. No jaundice. No spider angiomata or palmar erythema.
Neurologic: Alert and appropriate.  Answers questions and follows commands.  No asterixis.

LABS:
Na 129, K 3.9, Cl 93, CO2 27, BUN 14, Cr 0.96, Glu 106, Ca 8.6

ALT 15, AST 23, Alk Phos 131, Total bilirubin 0.5, Direct bilirubin 0.1

Amylase 41, Lipase 145, Albumin 2.3

WBC 6.8, Hb 9.2, Hct 28.9, Plt 583, MCV 72.6

APTT 30.4, PT 11.4, INR 1.06

Bedside ultrasound of the abdomen reveals significant free fluid in Morrison’s pouch.  A diagnostic and therapeutic paracentesis is performed, resulting in immediate return of cloudy yellow fluid. Four liters of peritoneal fluid are removed.  The patient’s discomfort is significantly relieved and her respiratory rate returns to normal. The peritoneal fluid is sent for analysis.

Questions:

#1 Which of the following is a contraindication to performing paracentesis?
a) pregnancy
b) disseminated intravascular coagulation
c) prolonged prothrombin time
d) thrombocytopenia

#2 Which of the following tests of the peritoneal fluid would be most helpful in determining the cause of the ascites?
a) pH
b) lactate
c) cholesterol
d) albumin

#3 The peritoneal fluid is analyzed and is positive for malignant cells. You suspect ovarian carcinoma. Which of the following serum tumor markers is associated with ovarian carcinoma?
a) CA-125
b) S-100
c) alpha fetoprotein
d) CEA

Answers & Discussion:

#1 Answer: b. disseminated intravascular coagulation
Many patients undergoing paracentesis have a prolonged prothrombin time or thrombocytopenia as a result of hepatic disease. These are not considered contraindications to performing paracentesis as the incidence of clinically significant bleeding complications in these patients is low.  In a retrospective study of over 4500 paracenteses, severe hemorrhage occurred in <0.2% of cases.  Although paracentesis should be performed with caution in pregnant patients, pregnancy is not a contraindication to paracentesis.

The indications for abdominal paracentesis include the evaluation of new onset ascites, the evaluation of a patient with existing ascites who is being admitted to the hospital for any reason, and the evaluation of a patient with ascites who has signs of clinical deterioration (fever, abdominal pain, hepatic encephalopathy, peripheral leukocytosis, decline in renal function, or metabolic acidosis).

The following are relative contraindications to paracentesis: disseminated intravascular coagulation, primary fibrinolysis, and massive ileus with bowel distension (unless the paracentesis is performed under ultrasound guidance).  If there are surgical scars present on the abdomen, then the needle should be inserted several centimeters away from the scars because the bowel may be adherent to the peritoneal wall at the site of the scar.

#2 Answer: d. albumin
The serum-ascites albumin gradient (SAAG) is equal to the serum albumin level minus the ascitic fluid albumin level.  In this case, the ascitic fluid albumin level is 2.6, so the SAAG is 2.3 – 2.6 = -0.3.  Etiologies of ascites that are related to portal hypertension will have a SAAG >1.1 and these include presinusoidal causes (splenic or portal vein thrombosis, schistosomiasis), sinusoidal causes (cirrhosis), and postsinusoidal causes (right heart failure, constrictive pericarditis, Budd-Chiari syndrome).   Etiologies of ascites that are not related to portal hypertension will have a SAAG <1.1 and these include nephrotic syndrome, tuberculosis, and malignancy with peritoneal carcinomatosis such as ovarian carcinoma. In this patient, the SAAG is <1.1, indicating that the ascites is not related to portal hypertension.

#3 Answer: a. CA-125
The presence of malignant cells in the peritoneal fluid suggests peritoneal carcinomatosis, which is typically caused by secondary peritoneal surface malignancies (ovarian, colorectal, pancreatic, uterine) or extra-abdominal tumors (lymphoma, lung, breast). Malignant ascites is a poor prognostic sign.  Tumor markers are not used as a primary means of diagnosing malignancy, but in a patient with evidence of malignancy, such as malignant cells present in ascites, tumor markers can help in identifying the site of the primary. Currently CA-125 is approved by the FDA only for monitoring response to therapy in women with known epithelial ovarian carcinoma. With regard to diagnosing ovarian carcinoma in postmenopausal women, elevated serum CA-125 has a sensitivity for ovarian cancer of 69-87% and has a specificity for ovarian cancer of 81-93%.  In this patient, the CT thorax/abdomen/pelvis revealed nodular changes of the pleura and peritoneum that possibly related to a metastatic process, but did not reveal a primary tumor.  We did obtain a CA-125 level for this patient which was markedly elevated, and although it is not specific for ovarian carcinoma, it did provide guidance for what type of further imaging to pursue.  In this case we obtained a pelvic ultrasound to attempt to better visualize the ovaries.

Discussion:
When a patient presents to the ED with new onset ascites, two of the main questions you need to answer are whether the fluid is infected and whether the ascites is related to portal hypertension.  Routine tests that should be ordered on all ascitic fluid include cell count and differential, albumin, and total protein.

The results of the cell count and differential will indicate whether the fluid is infected. While a fluid culture may take hours to days to return, a cell count should be available much earlier, allowing for early detection of infection and initiation of antibiotic therapy. You should consider starting antibiotics in any patient whose ascitic fluid corrected neutrophil count is greater than or equal to 250/mm3. One WBC should be subtracted from the WBC count for every 750 RBCs to reveal to corrected WBC count.  One neutrophil should be subtracted from the absolute neutrophil count for every 250 RBCs to reveal the corrected neutrophil count.

It is crucial not to miss spontaneous bacterial peritonitis in a patient with ascites who presents to the ED since shock and multi-system organ failure may occur rapidly if antibiotics are not promptly initiated. Patients with spontaneous bacterial peritonitis often present with fever, altered mental status, and diffuse abdominal pain. They may have lab findings including leukocytosis, metabolic acidosis, and azotemia.

As discussed above, the albumin level in the ascitic fluid, along with the serum albumin level, will allow you to calculate the serum-ascites albumin gradient and determine whether the fluid is related to portal hypertension or not.

If the total protein level in the ascitic fluid is greater than or equal to 2.5 g/dL, it is classified as an exudate. If it is less than 2.5, then it is a transudate.

Other tests that you should consider ordering for ascitic fluid include culture, glucose, lactate dehydrogenase, gram stain, and amylase.

Key Points:

• Consider paracentesis in any patient with new onset ascites or in any patient with existing ascites who is being admitted or exhibits signs of clinical deterioration.
• When you send ascitic fluid for analysis, always order cell count and differential, albumin, and total protein.
• Start antibiotics early if the corrected neutrophil count suggests spontaneous bacterial peritonitis.
• Calculate the serum-ascites albumin gradient to determine whether the ascites is related to portal hypertension or not

References:
Runyon BA et al. Ascitic fluid pH and lactate: insensitive and nonspecific tests in detecting ascitic fluid infection. 1991. Hepatology 13(5):929.

Runyon BA. Malignancy-related ascites and ascitic fluid ‘humoral tests of malignancy.’ 1994 J Clin Gastroenterol. 18(2):94.

Runyon BA. Evaluation of adults with ascites. UptoDate. 2013.

Sangisetty SL et al. Malignant ascites: a review of prognostic factors, pathophysiology, and therapeutic measures.  2012. World Journal of Gastrointestinal Surgery. 4(4): 87-95.

Thomsen TW et al. Paracentesis. 2006. New England Journal of Medicine 355:e21.

Intern Report 7.5

Case Presentation by Dr. Sean Teshima McCormick, MD

HPI:
The patient is a 74 year old male with a history of HTN, HLD who reports to the emergency department complaining of vision loss in his right eye 2 hours prior to presentation. The patient reports that he was sitting on his couch watching TV when it looked like someone was “turning down a dimmer switch” on the vision in his right eye. After a few seconds, it went completely black. He denies any pain at the time or currently. He denies any trauma. He denies seeing flashing lights, floating specs or cobwebs in his vision. He denies seeing anything that looked like a curtain coming over his vision. He reports no changes in his left eye. He denies any headaches, dizziness, focal numbness or weakness.

ROS:
Reports changes in his vision as described above
Denies fever, headache, chest pain, shortness of breath, N/V, diarrhea, constipation, dysuria, bleeding problems, new rashes

PMH: HTN, HLD
PSH: Left knee
Medications: HCTZ, simvastatin
Allergies: NKDA
FH: HTN, DM
SH: reports 1 pack per day tobacco use, reports occ alcohol use, denies any illegal drugs

Physical exam:
BP: 170/ 110 HR: 64 RR: 18 T: 37.0  Spo2: 99%
General: well-appearing thin man in no acute distress
Eyes: right pupil is round, shows afferent pupillary defect, left pupil is round and reactive, EOM intact bilaterally, painless, visual acuity is hand motion only right side, 20/40 on left, loss of confrontation fields on right eye, no conjuctival hemorrhage bilaterally, no signs of trauma
Cardiovascular: RRR, normal s1, s2
Respiratory: CTAB, no wheezes, crackles
Gastrointestinal:  abdomen soft, non-tender, non-distended, no organomegaly
Neurological: APD noted on right pupil, other CN intact, strength 5/5 bilaterally in upper and lower extremities, no sensory deficits
Musculoskeletal: no lower extremity edema
Skin: no rashes seen

Questions:

1) Based on the history and physical examination, what is the most likely diagnosis?
a) Retinal Detachment
b) Vitreous Hemorrhage
c) Amaurosis Fugax
d) Central Retinal Artery Occlusion
e) Pituitary tumor

2) What would you expect to see on fundoscopic exam?

3) Which diagnostic test should be ordered immediately?
a) Ocular Ultrasound
b) MRI Head and Brain
c) Carotid Duplex
d) Fluorescein Stain
e) Optical Coherence Tomography

 

Answers and Discussion:

1) D. Central Retinal Artery Occlusion.
CRAO causes sudden painless monocular vision loss. Patients often describe the vison loss as someone slowly dimming their vision until it is completely black. These patients will only be able to see hand motions out of the affected eye and will have an afferent pupillary defect. The most common risk factors for CRAO are HTN, HLD and smoking. Patients with a retinal detachment can also experience a sudden painless monocular vision loss. However, these patients will often describe flashing lights and floating specs, thought to be caused by nonspecific stimulation of the retina as it detatches. They will describe their visual field as obscured by a moving curtain. They should still have parts of their visual field intact. Patients with vitreous hemorrhage will decribe their vison as seeing “cobwebs.” This is usually a progression of diabetic disease or the result of trauma. Amaurosis fugax is by definition a transient phenomenon and often is resolved by the time the patient presents to a healthcare professional. Pituitary tumor will cause a bitemporal hemianopsia, not a monocular vision loss.

2) B.
CRAO is caused by the occulsion of  the central retinal artery, which supplies the portion of the retina responsible for central vision. In this image, since the artery is occluded, the central retina is pale. A “cherry red spot”  is seen at the macula. This occurs because the retina is thinner at the macula and the retinal pigment and choroid vessels can be seen. Additionaly, some people have addional blood supply to the macula that may result in a small area of preserved vision known as macular sparing. Image A is a branch retinal artery occlusion. Here you can see the area of pallor is confined to smaller distribution in the inferior portion of the retina instead of the entire central vision. Image C is a retinal detachment. Image D is a vitreous hemorhage. Image E is a normal retina. In contrast to image B, here you can see good blood supply to the central retina.

3) C. Carotid Duplex
The most common cause of CRAO is ipsilateral carotid artery athlerosclerosis. Since these patients are at risk of stroke, carotid duplex must be ordered emergently. Cardiogenic embolism is the second most common cause so an EKG should also be ordered. An echocardiogram should be considered if there are significant risk factrors. Risk factors for cardiogenic source include atrial fibrillation, endocarditis, valvular disease, MI, IVDA. An ocular ultrasound would aid in the diagnosis of retinal detachment. An MRI would aid in the diagnosis of intracranial mass. A fluorescein stain would aid in the diagnosis of corneal abrasion. OCT would aid in the diagnosis of macular degneration, macular edema and epiretinal membrane.

Summary:
CRAO will present as sudden painless monocular vision loss that patients describe as “dimming” of their vision. This is an emergency due to the risk of stroke. Patients with HTN, HLD and smoking are at greater risk. On physical exam, patients will have an APD in the affected eye and will often only be able to make out hand movements. Diagnosis is made by fundoscopic examination which reveals a pale central retina often with macular sparing which appears as a “cherry red spot.” Since carotid artery atherosclerosis and cardiogenic emboli are the most common etiologies, there is concern for cerebral vascular accident. A work up should include carodtid duplex and EKG, and possibly an echocardiogram. 10-15% of CRAO are associated with giant cell arteritits so a CRP and ESR should also be ordered. Vasculitis, sickle cell disease and hypercoagulable states are less common causes. Therefore, hematologic and coagulation studies should also be considered. Currently there is no standard treatment, however several therapies have been associated with better outcomes. Ocular massage and anti-platelet therapy may be initiated to help restore blood flow. Hyperbaric oxygen therapy has also been shown to improve outcomes in CRAO and Detroit Receiving Hospital is a hyperbaric referral center. Other experimental therapies include thrombolytics, mannitol to decrease intraocular pressure and nitroglycerin to increase bloodflow.

Intern Report 7.4

Case Presentation by Dr. Nile Chang, MD

A 29 year old African-American pregnant female, G3P2, 38 weeks pregnant per LMP, presents with 2 weeks of progressively worsening shortness of breath and dyspnea with exertion, orthopnea, and ankle edema. She also reports occasional cough worse when she lies down. She reports having gained 15 pounds over the last month. She saw her OBGYN about a month ago and “everything has been fine”.  Her previous pregnancies were notable for full-term vaginal births without complications. She denies fevers, chills, vomiting, headache, or rash.

PMH:
No significant medical history
No significant surgical history
Allergies: no known drug allergies

Physical exam:

General: In mild distress, tachypneic
Vitals: T – 97.6 Pulse- 80 RR- 28 BP- 170/85 O2Sat-88% on RA
HEENT: Normocephalic, Atraumatic, PERRLA, no JVD or distended neck veins
Respiratory: Breath sounds clear and equal bilaterally, no wheezes, rhonchi, or rales, no accessory muscle use
Cardiac: Regular rhythm and rate, no murmurs, rubs or gallops
Abdomen: Gravid, non-tender, soft, no rigidity, rebound, or guarding
Skin: Warm and dry without diaphoresis
Extremities: Palpable pulses in equal bilaterally in all extremities. 2+ pitting edema in both lower extremities
Neurologically: A&Ox3, normal speech, symmetrical strength, DTRs 2+ at the patella and symmetrical, no clonus

Labs:

WBC: 10.2
HGB: 11.3
Plt: 335

Na: 133
K: 4.0
Cl: 100
HCO3: 22
BUN: 13
Cr: 1.2

Alb: 3.2
TP: 8
T.Bili: 0.3
D Bili: 0.1
ALT: 35
AST: 50
Alk Phos: 165

pH: 7.43
pCO2: 27
PO2: 56
FiO2:21

Urinalysis: normal

Fetal Doppler: 132 bpm

Questions:

Q1. Which of the following findings is least likely to be found on echocardiogram for this patient?
a) Dilated Left Ventricle
b) Reduced diastolic filling
c) Reduced LV ejection fraction
d) Small pericardial effusion

Q2. Which of the following imaging study exposes the fetus to the most amount of ionizing radiation?
a) Chest X-ray
b) Pelvis X-ray
c) CT Pulmonary Angiogram with abdominal shielding
d) V/Q Scan

Q3. Which one of the following pharmacotherapy should not be used to manage this patient?
a) Beta-blocker
b) ACE inhibitor
c) Hydralazine
d) Furosemide

Answers & Discussion:

1) B
2) B
3) B

Dyspnea in pregnancy is a common complaint seen in the ED. Normal physiological changes includes a normal increase in minute ventilation, which often presents as a complaint. However, dyspnea can be a harbinger for several life-threatening emergencies that require prompt evaluation. These emergencies include asthma, pneumonia, pulmonary embolism, and pulmonary edema secondary to preeclampsia or dilated cardiomyopathy.

The patient in this case has a clear clinical picture of pulmonary edema secondary to peripartum dilated cardiomyopathy (PPCM). Her history and physical is notable for worsening shortness of breath, ankle edema, orthopnea, and paroxysmal nocturnal dyspnea, all signs of heart failure. PPCM generally occur in the last month of pregnancy or within the first five months of delivery.

Q1.  Answer: B

PPCM is a dilated, high output form of cardiac failure. Of the answer choices, findings of a dilated left ventricle (a) and reduced LV ejection fraction (c) on echocardiogram is a definitive diagnosis. A small pericardial effusion can also be seen (d). Reduced diastolic filling (b) is more associated with a restrictive cardiomyopathy, not generally seen in PPCM.

In this patient, additional evaluation such as a BNP may also help confirm the diagnosis.

Q2.  Answer: B

When considering radiological imaging in the pregnant patient, one must be cognizant of the potential exposure of ionizing radiation to the developing fetus, and weigh the risk of the exposure against the risk of misdiagnosis.

The ACOG technical bulletin suggest that significant risk is unlikely when the fetus is exposed to less than 100 rads of cumulative radiation during pregnancy. With exposure to 15 rads or greater, there is a 6% chance of severe mental retardation and 15% chance of microsomia. The following table lists the estimated radiation dose to the fetus by imaging modality.

C-spine (<1mrad)
Chest X-ray (1-3 mrad)
KUB (200-500 mrad)
Pelvis X-ray (200-500 mrad)
L-spine (600-1000mrad)
CT Head/Chest (with shielding) (<1000 mrad)
CT Abdomen (3000 mrad)
CT Pelvis (3000-9000 mrad)
V/Q scan (<55 mrad)
CT PE (with shielding) (<50 mrad)

Conventional wisdoms suggest that a V/Q scan was the test of choice to rule out PE, however, more recent studies have shown that CT with PE protocol may provide a similar level of exposure while providing a higher level of sensitivity and specificity. Therefore, pregnancy should not preclude the use of helical CT for the diagnosis or rule-out of PE.

Of the answer choices, a pelvis X-ray (b) have a highest level of exposure (200-500mrad).

Q3.  Answer: B

For the most part, the goals of medical therapy are similar to those in patients with heart failure due to other causes. However, ACE inhibitors (b) and ARBs are contraindicated at any time in pregnancy. However, they are safe to use in women who are breastfeeding.

Because ACE Inhibitors and ARBS are contraindicated in pregnancy, hydralazine (c) is a safe option for antepartum vasodilation and blood pressure reduction.

Beta-blockers (a) are generally safe during pregnancy, with agents that are beta-1 selective (metoprolol) are preferable, as ones that are not (atenolol) may interfere with beta-2 mediated uterine relaxation and peripheral vasodilation.

Diuretics such as furosemide (d) and hydrochlorothiazide should only be used if there are signs of pulmonary congestion, as it may decrease blood flow over the placenta.

References:
1. Rosen’s Emergency Medicine, Concepts and Practices, 7^th edition

2. Trauma during pregnancy: ACOG technical bulletin. American College of Obstetricians and Gynecologists. November 1991.

3. ESC Guidelines on the management of cardiovascular diseases during pregnancy. European Heart Journal (2001) 32, 3147-3197

4. Peripartum Cardiomyopathy. UpToDate. Wolters Kluwer Health. 2013.