Fever in Systemic Lupus Erythematosus

HPI:

48F with a history of SLE presenting with two weeks of fevers and joint pain. The patient reports progressive development of these symptoms associated with malaise and muscle aches. She also reports two days of cough productive of yellow sputum, but denies chest pain, shortness of breath or hemoptysis. She states that these symptoms are comparable to prior lupus flares but have persisted longer than usual. She has not travelled or been hospitalized recently and has no sick contacts.

PMH:

SLE
AVN left hip

PSH:

Total hip arthroplasty

FH:

Non-contributory

SHx:

Denies tobacco, alcohol or drug use.
Works as an accountant.
No history of TB exposure.

Meds:

Methotrexate 50mg p.o. weekly
Plaquenil 400mg p.o. daily
MVI

Allergies:

NKDA

Physical Exam:

VS:	T	39.4	HR	138	RR	19	BP	97/61	O2	98% 2L NC
Gen:	Alert, responsive and in no acute distress.
HEENT:	PERRL, dry mucous membranes, no oropharyngeal lesions or erythema, TM intact bilaterally, no cervical lymphadenopathy, neck supple.
CV:	Tachycardia, regular rhythm without additional heart sounds.
Lungs:	Clear to auscultation bilaterally.
Abd:	+BS, soft, non-tender, non-distended, no rebound/guarding.
Ext:	No peripheral edema, extremities warm and well-perfused, diffuse tenderness to palpation and resisted range of motion of joints with particular involvement of bilateral shoulders, elbows, knees and ankles. No effusion noted, no erythema or warmth.
Neuro:	Alert, oriented to self, location and time. PERRL, EOMI, facial sensation intact, facial muscles symmetric, palate rises symmetrically, tongue protrudes midline without fasciculation, peripheral sensation and motor strength grossly intact with normal gait.

Labs/Studies:

0h:
CBC: 6.0/7.7/23.5/259
BMP: 138/2.8/116/18/12/0.66/71
Ca: 5.0 (corrected for hypoalbuminemia: 6.9)
Mg: 1.1
Lactate: 0.7
ESR: 81 (0-20)
CRP: 7.99 (0-0.74)
C3: 60 (79-152)
C4: 13 (16-38)

12h:
BMP: 142/4.6/113/26/15/0.75/128
Ca: 7.8

Imaging:

CXR: Negative for acute cardiopulmonary process.

Assessment/Plan:

48F with a history of SLE presenting with fever and polyarticular arthralgia.

#SIRS: Fever and tachycardia in the setting of immunosuppression. The differential diagnosis includes pneumonia (bacterial, viral, less-likely fungal), which would be community-acquired. Association with polyarticular arthralgia suggests symptoms may represent lupus flare given no leukocytosis and elevated CRP.

#Hypocalcemia: Asymptomatic, likely due to hypoalbuminemia and hypomagnesemia. Improved after IV fluids and correction of hypokalemia, hypomagnesemia.

Hospital Course:

The patient was admitted and completed a 7-day course of ceftriaxone and azithromycin. Rheumatology was consulted for management of lupus flare, which included resuming home medications and a prednisone taper upon discharge.
The patient was admitted ten days later, presenting with fevers, productive cough and pleuritic chest pain. Found to have a left lower lobe sub-segmental pulmonary embolus and antiphospholipid syndrome. She was also treated empirically for healthcare-associated pneumonia with cefepime and vancomycin given fever and productive cough though there were no imaging findings suggestive of consolidation and sputum cultures were negative.

Differential Diagnosis of Hypocalcemia: ^1,2

Laboratory Evaluation of Hypocalcemia: ^1,2

Clinical Manifestations of Hypocalcemia: ¹

Neuromuscular
- Hyperexcitability
- Perioral paresthesias
- Muscle weakness, cramps, fasciulations, tetany
CNS
- Depression
- Irritability
- Confusion
- Seizure
Cardiac
- Decreased contractility/conduction
- QT prolongation

Management of Symptomatic Hypocalcemia: ¹

10mL 10% Calcium Gluconate
Dilute in 100mL D5W

Fever in SLE:

It is important to differentiate whether fever in a patient with SLE is due to disease activity (flare) or active infection.

Risk Factors for Infection:³

Neutropenia/Lymphopenia
Hypocomplementemia
Immunosuppressive therapy (especially Azathioprine⁴)

Laboratory Studies:³

CRP: sensitivity 100%, specificity 90% >1.35mg/dL ⁵
PCT: sensitivity 75%, specificity 75% ⁶

References:

Cooper, M. S., & Gittoes, N. J. L. (2008). Diagnosis and management of hypocalcaemia. BMJ (Clinical research ed.), 336(7656), 1298–1302. doi:10.1136/bmj.39582.589433.BE
Hannan, F. M., & Thakker, R. V. (2013). Investigating hypocalcaemia. BMJ (Clinical research ed.), 346(may09 1), f2213–f2213. doi:10.1136/bmj.f2213
Cuchacovich, R., & Gedalia, A. (2009). Pathophysiology and clinical spectrum of infections in systemic lupus erythematosus. Rheumatic diseases clinics of North America, 35(1), 75–93. doi:10.1016/j.rdc.2009.03.003
Zhou, W. J., & Yang, C.-D. (2009). The causes and clinical significance of fever in systemic lupus erythematosus: a retrospective study of 487 hospitalised patients. Lupus, 18(9), 807–812. doi:10.1177/0961203309103870
Kim, H.-A., Jeon, J.-Y., An, J.-M., Koh, B.-R., & Suh, C.-H. (2012). C-reactive protein is a more sensitive and specific marker for diagnosing bacterial infections in systemic lupus erythematosus compared to S100A8/A9 and procalcitonin. The Journal of rheumatology, 39(4), 728–734. doi:10.3899/jrheum.111044
Scirè, C. A., Cavagna, L., Perotti, C., Bruschi, E., Caporali, R., & Montecucco, C. (2006). Diagnostic value of procalcitonin measurement in febrile patients with systemic autoimmune diseases. Clinical and experimental rheumatology, 24(2), 123–128.

Electrolyte Abnormalities

Routine laboratory studies are common in the intensive care unit; abnormalities are even more common. Typically these studies include a chemistry panel (Chem 10). The differential diagnoses of the most frequent and clinically relevant electrolyte abnormalities are detailed below.

Differential Diagnosis and Evaluation of Hyponatremia

Differential Diagnosis and Evaluation of Hypernatremia

Differential Diagnosis and Evaluation of Hypokalemia

Differential Diagnosis of Hyperkalemia

Differential Diagnosis of Hypo and Hypercalcemia

Differential Diagnosis of Hypo and Hypermagnesemia

Differential Diagnosis of Hypo and Hyperphosphatemia

References:

Marino, P. (2014). Marino’s the ICU book. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Fulop, M. (1998). Algorithms for diagnosing some electrolyte disorders. American Journal of Emergency Medicine, 16(1), 76–84.
WikEM: Hypokalemia
WikEM: Hyponatremia

Biliary Duct Dilation

A 45 year-old male presents with progressive jaundice over 1 month, he denies abdominal pain.

Ultrasound

CT Abdomen/Pelvis

Markedly dilated intrahepatic biliary ducts, common bile duct and pancreatic duct.
Ill-defined fullness in the pancreatic head consistent with pancreatic adenocarcinoma vs. noncalcified obstructing biliary stone.

Differential Diagnosis of Biliary Duct Dilation: ^1,2,3

References:

Kim, H. J., Lee, K. T., Kim, S. H., Lee, J. K., Lim, J. H., Paik, S. W., & Rhee, J. C. (2003). Differential diagnosis of intrahepatic bile duct dilatation without demonstrable mass on ultrasonography or CT: benign versus malignancy. Journal of gastroenterology and hepatology, 18(11), 1287–1292.
Levy, A. D. (2009). Biliary Ducts – Pathology. The Radiology Assistant, 1–4. Retrieved from http://www.radiologyassistant.nl/en/p49e17de25294d/biliary-ducts-pathology.html
Teefey, S. A., Baron, R. L., Schulte, S. J., Patten, R. M., & Molloy, M. H. (1992). Patterns of intrahepatic bile duct dilatation at CT: correlation with obstructive disease processes. Radiology, 182(1), 139–142. doi:10.1148/radiology.182.1.1727277

Acute Kidney Injury

Hospital Course:

64 year-old female with a history of metastatic colonic adenocarcinoma was initially admitted for PO intolerance secondary to recurrent small bowel obstructions (associated with abdominal tumor burden). On hospital day six, the patient developed tachypnea, hypoxemia, hypotension and was intubated for respiratory distress. In the MICU, the patient was treated for acute hypoxic respiratory failure thought to be caused by aspiration (large volume bilious emesis prior to intubation despite NGT LCWS) vs. accumulating malignant pleural effusions vs. pulmonary embolism. Septic shock of a presumed pulmonary vs. intra-abdominal source was managed with vasopressors and broad-spectrum antimicrobials.

On hospital day fourteen, an elevation in the serum creatinine was noted. Known nephrotoxic agents include iodinated contrast on hospital day five, and vancomycin. The patient’s vasopressor requirement had decreased to norepinephrine 6mcg/kg/min (previously requiring four vasopressors). Over the next six days, the serum creatinine continued to trend upwards associated with a decrease in urine output (0.3-0.5mL/kg/hour). Intravenous crystalloid and colloid administered liberally based on central venous pressure and ultrasound of the inferior vena cava did not impact urine output.

Laboratory Studies

Hospital day	19	18	17	16	15	14	3
Creatinine	1.72	1.59	1.46	1.32	1.24	1.09	0.75
Vancomycin	23.5	28.5	36.3	45.5	47.7		22.1

Urine electrolytes:

Una: 10
Ucr: 180
Uk: 13
Ucl: 22
Uur: 265
FeNa: <1%

UA: 3+LE, 1+ blood, 36WBC, 14RBC, 3+ bacteria, amorphous crystals

Imaging:

CT Abdomen/Pelvis with IV contrast

Within the retroperitoneum, the left kidney is small and atrophic and demonstrates limited peripheral enhancement. The left renal artery is also poorly visualized.
Severely dilated loops of small bowel, including a segment within the left lower quadrant that may represent a closed loop obstruction.
There is a large (16.4 cm in largest diameter) subphrenic fluid collection in the left upper quadrant. A second large (14.2 cm in largest diameter) intraabdominal fluid collection lies inferior and anteriorly.

Assessment:

Oliguric acute renal failure in the setting of convincingly pre-renal urine studies which was not responsive to adequate crystalloid and colloid volume resuscitation. The patient had a normal ejection fraction on a recent echocardiogram, and while the patient was hypoalbuminemic (presumably from poor nutritional status and PO intolerance), urine output was not even transiently responsive to colloid administration. While the patient had recent administration of intravenous contrast, the elevation in serum creatinine occurred more than one week later. Further, the elevated vancomycin trough was likely a consequence rather than the etiology of worsening renal failure. AKI was likely secondary to renal artery compression from mass effect associated with abdominal metastases. There was evidence of a similar process affecting the left kidney, which was severely atrophic. The patient declined further evaluation, which would have included a renal ultrasound.

Definition of Acute Kidney Injury: ¹

Elevation of serum creatinine > 0.3mg/dL in 48h
Elevation of serum creatinine > 1.5x baseline in 7d
Oliguria (UOP < 0.5mL/kg/hr) > 6h

Staging of Acute Kidney Injury: ¹

Stage	Creatinine	UOP
1	1.5-1.9x	<0.5mL/kg/hr for 6-12h
2	2.0-2.9x	<0.5mL/kg/hr for >12h
3	3.0x or RRT	<0.3mL/kg/hr for > 24h

Management of Contrast-induced AKI: ²

Administer lowest dose
Use iso-osmolar, or low-osmolar contrast
Volume expansion (NaCl, NaHCO3)
PO NAC questionable benefit but likely harmless

Differential Diagnosis of Acute Kidney Injury: ³

NOTE: Algorithm revised in November, 2017. The prior version is no longer supported but remains available here.

Evaluation of AKI: ⁴

Condition	Urinalysis	Casts	FeNa (%)
Pre-renal	Normal	Hyaline	<1
Intra-renal
ATN	Mild proteinuria	Pigmented granular	>1
AIN	Mild proteinuria, Hb, WBC	WBC casts, eosinophils	>1
GN	Moderate/severe proteinuria, Hb	RBC casts	<1
Post-renal	Normal	Crystals	>1

References:

Kellum, J. A., Lameire, N., KDIGO AKI Guideline Work Group. (2013). Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical care (London, England), 17(1), 204. doi:10.1186/cc11454
Lameire, N., Kellum, J. A., KDIGO AKI Guideline Work Group. (2013). Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (Part 2). Critical care (London, England), 17(1), 205. doi:10.1186/cc11455
Lameire, N., Van Biesen, W., & Vanholder, R. (2005). Acute renal failure. Lancet, 365(9457), 417–430. doi:10.1016/S0140-6736(05)17831-3
Thadhani, R., Pascual, M., & Bonventre, J. V. (1996). Acute renal failure. New England Journal of Medicine, 334(22), 1448–1460. doi:10.1056/NEJM199605303342207
WikEM: Acute kidney injury

Ectopic Pregnancy

HPI:

32F G8P7A2 at 5 weeks by LMP presenting with abdominal pain. The patient reports acute onset of sharp left lower abdominal pain 1.5 hours prior to presentation. The pain has been constant since onset, 10/10 in severity, radiating to lower back and exacerbated with movement. She denies vaginal bleeding or discharge, passage of clots or other products. She also denies trauma, lightheadedness/dizziness/syncope, shortness of breath, nausea/vomiting or changes in bowel or urinary habits.
Her pregnancy was detected 3 weeks ago with a home pregnancy test and was confirmed at her PCP one week later. She has not had an ultrasound during this pregnancy but has a history of uterine fibroids. She has no history of sexually transmitted infections, prior ectopic pregnancy, or use of assisted fertilization.

PMH:

HTN
Uterine fibroids

PSH:

None

FH:

Non-contributory

SHx:

Denies tobacco, alcohol or drug use.
Sexually active with husband only, no history of STI.

Meds:

None

Allergies:

NKDA

Physical Exam:

VS:	T	37.4	HR	108	RR	36	BP	148/104	O2	99% RA
Gen:	Alert and oriented female, appears uncomfortable due to pain.
HEENT:	PERRL, EOMI, MMM.
CV:	Tachycardia, regular rhythm, no murmurs.
Lungs:	CTAB, no crackles.
Abd:	Normoactive bowel sounds, tenderness to palpation in LLQ and suprapubic area, with guarding but no rebound tenderness. No CVAT.
GU:	No external lesions. Closed cervical os, no blood or discharge, +CMT.
Ext:	Warm, well-perfused with strong peripheral pulses.

Labs/Studies:

POC Hemoglobin: 11.8
POC ICON: positive

Imaging:

Bedside Ultrasound

Transabdominal: Free fluid in hepatorenal and splenorenal recesses
Transvaginal: Free fluid and debris in posterior cul-de-sac, likely pseudogestational sac in endometrial cavity, no IUP identified. Formal ultrasound revealed fetus with cardiac activity in left adnexa.

Hepatorenal free fluid

Free fluid in the hepatorenal recess (Morison's Pouch)

Splenorenal Free Fluid

Free fluid in the splenorenal recess.

Pelvic Free Fluid

Free fluid and debris in the posterior cul-de-sac.

Pseudogestational Sac

No obvious yolk sac or fetal pole.

Assessment/Plan:

32 year-old ICON positive female with acute-onset pelvic pain. The patient remained hemodynamically stable and absence of definitive IUP on bedside ultrasound was confirmed with presence of fetal cardiac activity in left adnexa indicative of ectopic pregnancy. OB-Gyn was consulted and the patient was taken emergently to the OR.

Differential Diagnosis of First Trimester Abdominal Pain: ¹

Initial Evaluation of First Trimester Abdominal Pain: ¹

2 large-bore IV’s, begin fluid resuscitation
POC testing: hemoglobin, urine pregnancy
CBC, type and cross (Rh), serum B-hCG
Emergent bedside ultrasound

Features Associated with Ectopic Pregnancy: ¹

History

PID
Tubal ligation
Prior ectopic
IUD
Assisted fertilization

Physical

CMT
Peritoneal irritation

Ultrasound

Empty uterus
Adnexal mass
Free fluid

Ultrasonographic Findings in the Evaluation of Ectopic Pregnancy: ²

Discriminatory hCG (1500-3000 mIU/mL): absence of IUP suggests ectopic or abnormal gestation
Normal IUP
- 4-5wks: gestational sac (0.2-0.5cm)
- 5wks: two echogenic rings
- 5.5wks: yolk sac
- 6wk: embryonic pole
- 6.5wk: fetal cardiac activity
Abnormal IUP
- >2cm gestational sac without fetal pole
- CRL >0.5cm without cardiac activity
Ectopic
- Extrauterine gestational sac with or without cardiac activity
- Extrauterine ring sign
- Non-homogenous adnexal mass

Contraindications to Medical Management: ^2,3

Absolute
- Breast-feeding
- Immunodeficiency
- PUD
- Pulmonary, hepatic or renal dysfunction
Relative
- Ectopic mass > 3.5cm
- Fetal cardiac activity

References:

Dart, R. (2003). First Trimester Emergencies A Practical Approach To Abdominal Pain And Vaginal Bleeding In Early Pregnancy. EB Medicine, 5(11), 1–20.
Barnhart, K. T. (2009). Clinical practice. Ectopic pregnancy. The New England journal of medicine, 361(4), 379–387. doi:10.1056/NEJMcp0810384
Jurkovic, D., & Wilkinson, H. (2011). Diagnosis and management of ectopic pregnancy. BMJ (Clinical research ed.), 342(jun10 1), d3397–d3397. doi:10.1136/bmj.d3397

Ultrasound Gallery

Appendicitis

Non-compressible tubular structure in the RLQ of a patient with focal abdominal tenderness. >6mm in diameter.

Common Bile Duct

A tubular structure typically anterior to the portal vein without flow. Normally measures <4mm, increases by 1mm per decade after 40yrs.

Cellulitis

"Cobblestone" appearance of soft tissue suggesting infection/edema.

Fetal Heart Rate

Placing the M-Mode marker over the most visibly active portion of the fetal heart allows for measurement of the fetal heart rate.

Free Fluid

Free fluid in the hepatorenal recess.

Hydronephrosis

Severe hydronephrosis.

Thoracic Aorta Aneurysm

Subxiphoid view of thoracic aorta, markedly dilated (>3cm) with thrombus.

Pericardial Effusion

Mild pericardial effusion in a patient with pleuritic chest pain.

Inferior Vena Cava

IVC without significant respiratory variation.

B-lines

B-lines extending deep from pleura suggestive of interstitial fluid accumulation (pulmonary edema).

"Shred" sign

Irregular, "shredded" pleural line suggestive of consolidation.

Pneumothorax

Transition point with loss of lung sliding in a patient with a small spontaneous pneumothorax.

Lower Extremity Edema

HPI:

51 year-old male with a history of HTN, DM and chronic alcohol abuse presenting with lower extremity swelling. He notes one month of progressive, bilateral lower extremity swelling, in the past two weeks associated with increasing pain and redness and is now no longer able to ambulate due to pain. He denies fevers/chills, chest pain or shortness of breath. He also denies orthopnea and paroxysmal nocturnal dyspnea. He states that he has not had these symptoms prior to one month ago. On review of systems he denies nausea/vomiting, abdominal pain, and changes in bowel or urinary habits. He has a history of GI bleeding (unknown treatment) but denies hematemesis, hematochezia or melena. He has previously experienced alcohol withdrawal, which manifested as tremors, but no hallucinations or seizures.

PMH:

HTN
DM
Chronic EtOH abuse

PSH:

None

FH:

Unknown

SHx:

Drinks 1-2 pints of alcohol daily, last drink this morning.
Denies current tobacco or drug abuse, no prior IVDA.

Meds:

None

Allergies:

NKDA

Physical Exam:

VS:	T	37.6	HR	86	RR	16	BP	128/84	O2	99% RA
Gen:	Adult, non-obese male, lying in bed. Tremors noted in upper extremities.
HEENT:	PERRL, EOMI, no scleral icterus. Mucous membranes moist.
CV:	RRR, normal S1/S2, no additional heart sounds, JVP 3cm above sternal angle at 30°.
Lungs:	CTAB, no crackles.
Abd:	Soft, non-distended, with normoactive bowel sounds. Liver edge palpated 1cm below costal margin at mid-clavicular line, non-tender. No rebound/guarding.
Ext:	Warm, well-perfused with 2+ distal pulses (PT, DP). 3+ pitting edema symmetric in bilateral lower extremities to knee. Erythema and warmth bilaterally extending from ankles to mid-shin. Mild tenderness to palpation. No pain with passive dorsiflexion. 3x3cm shallow ulceration below medial malleolus on right lower extremity without underlying fluctuance or expression of purulent material. No venous varicosities noted. Decreased sensation to light touch below knee bilaterally.
Rectal:	Normal rectal tone, brown stool, guaiac negative.
Neuro:	Alert and oriented, CN II-XII intact, gait intact, normal FTN/RAM.

Labs/Studies:

CBC: 7.4/13.1/39/180
Creatinine: 0.84
Albumin: 4.3
BNP: 28

Imaging:

Venous Lower Extremity Ultrasound

No DVT.
Pulsatile flow in bilateral EIV (external iliac veins) suggestive of elevated right heart pressure.

Assessment/Plan:

51M with HTN, DM, EtOH abuse presenting with lower extremity edema. Chronic bilateral lower extremity edema likely secondary to chronic venous insufficiency perhaps related to OSA given ultrasound findings of pulsatile flow in EIV’s. Doubt systemic cause: no evidence of heart failure on exam and normal BNP, no stigmata of cirrhosis and normal albumin, normal creatinine. Also, no evidence of DVT on ultrasound though bilateral DVT unlikely. Bilateral cellulitis also unlikely as the patient is afebrile without leukocytosis, however the patient was started on antibiotics including ceftriaxone and TMP/SMX given erythema, warmth and tenderness to palpation. The patient received benzodiazepines which eased withdrawal symptoms and he was admitted for continued treatment.

Mechanisms of Lower Extremity Edema: ¹

Differential Diagnosis of Lower Extremity Edema: ^1,2

Evaluation:

History ^1,2

Duration: acute (<72h) vs. chronic
Pain: DVT, CRPS, less severe in venous insufficiency
Systemic Disease
- Cardiac: orthopnea, PND
- Renal: proteinuria
- Hepatic: jaundice, ascites
Malignancy: lymphedema
Improvement with elevation/recumbency: venous insufficiency
OSA: snoring, daytime somnolence
Medications: B-blocker, CCB, hormones, NSAID’s

Physical Exam ^1,2

Distribution: unilateral, bilateral, generalized
Quality: pitting, non-pitting
TTP: DVT, cellulitis
Varicose veins: venous insufficiency
Kaposi-Stemmer: inability to pinch dorsum of foot at base of 2nd toe (lymphedema)
Systemic Disease
- Cardiac: JVD, crackles
- Hepatic: ascites, scleral icterus, spider angiomas
Brawny, medial maleolar involvement: venous insufficiency

Key Features Distinguishing Cellulitis: ³

Typically unilateral and acute
Often with systemic symptoms (fever, leukocytosis)
Risk Factors: immunosuppression, previous episodes, DM, PVD

References:

Trayes, K. P., Studdiford, J. S., Pickle, S., & Tully, A. S. (2013). Edema: diagnosis and management. American family physician, 88(2), 102–110.
Ely, J. W., Osheroff, J. A., Chambliss, M. L., & Ebell, M. H. (2006). Approach to leg edema of unclear etiology. Journal of the American Board of Family Medicine : JABFM, 19(2), 148–160.
Keller, E. C., Tomecki, K. J., & Alraies, M. C. (2012). Distinguishing cellulitis from its mimics. Cleveland Clinic journal of medicine, 79(8), 547–552. doi:10.3949/ccjm.79a.11121
WikEM: Pedal edema

Lymphadenopathy Applied: Lymphoma

HPI:

27 year-old female with no medical history presenting with neck swelling. She describes one month of progressive enlargement of a left-sided neck mass, and in the past two weeks has noted a new right-sided neck mass. This has been associated with worsening dysphagia to solids, describing a sensation of food lodging in the mid-chest and requiring liquids for passage – she attributes her recent 10lb weight loss to this. She also reports a non-productive cough for the past two weeks and generalized fatigue. She otherwise denies fevers, night sweats, chest pain, shortness of breath, nausea/vomiting, or changes in bowel/urinary habits. She has no known sick contacts or TB exposure risk factors. She has no medical history, no prior surgeries, does not take any medications and denies tobacco, alcohol or drug use.

Physical Exam:

VS:	T	38.4	HR	98	RR	14	BP	108/68	O2	99% RA
Gen:	Well-appearing young female, in no acute distress.
HEENT:	PERRL, EOMI, MMM without lesions. There is a 2x3cm firm, non-tender, mobile left supraclavicular lymph node, as well as two 1x1cm firm, non-tender lymph nodes in the left and right anterior cervical chains.
CV:	RRR, normal S1/S2, no murmurs. No JVD.
Lungs:	Clear to auscultation bilaterally. There is a transition to bronchial breath sounds along the trachea inferior to the sternal angle with normal tracheal sounds superiorly.
Abd:	Soft, non-tender without organomegaly.
Ext:	Warm and well-perfused with normal peripheral pulses. No axillary or inguinal lymphadenopathy.
Neuro:	Alert and oriented, responding appropriately to questions. PERRL, EOMI, facial sensation symmetric, facial muscles symmetric, hearing grossly normal, palate rises symmetrically, tongue movements normal without fasciculation, SCM/trapezius normal. Normal FTN, RAM. Gait intact. Peripheral sensation and motor grossly normal.

Imaging:

CT Chest - Axial

Anterior mediastinal mass with a wide differential - likely represents lymphoma or germ cell tumor. Less likely thymic or thyroid origin.

CT Chest - Sagittal

Anterior mediastinal mass with a wide differential - likely represents lymphoma or germ cell tumor. Less likely thymic or thyroid origin.

Assessment/Plan:

27F with no PMH presenting with progressive localized lymphadenopathy. Resultant dysphagia, cervical and supraclavicular distribution as well as abnormal tracheal sounds concerning for mediastinal involvement. The patient is currently stable without evidence of airway compromise. A CT of the chest was obtained to evaluate for thoracic malignancy, which showed a large anterior mediastinal mass concerning lymphoma or germ cell tumor. The location of the mass likely explains the patient’s dysphagia due to compression of the esophagus, as well as the abnormal pulmonary exam with compression potentially irritating the trachea and triggering her non-productive cough. The patient was admitted for further workup.

Lymphadenopathy Applied – Lymphoma

This case applies the differential diagnosis of lymphadenopathy. The most abnormal finding on examination was non-tender, left supraclavicular lymphadenopathy. The duration of symptoms and lack of tenderness is concerning for malignancy, and the left supraclavicular location suggests a thoracic or intra-abdominal source.

Necrotizing Soft-Tissue Infection (NSTI)

HPI:

40 year-old male with a history of diabetes presents with right foot pain and swelling. His symptoms began 3 days ago with pain on the lateral surface of his right foot, described as aching, non-radiating and exacerbated with walking. Yesterday, he noted more prominent swelling and redness involving 4th and 5th toes. He denies trauma, fevers, and discharge.

PMH:

Diabetes mellitus, diagnosed 8yrs ago

PSH:

None

FH:

Non-contributory

SHx:

Lives with wife and 2 children and works an office job.
Ten year history of tobacco use, quit 3 years ago.
No EtOH or drug abuse.

Meds:

Metformin 500mg p.o. b.i.d.
Ibuprofen p.r.n. joint pain

Allergies:

NKDA

Physical Exam:

VS:	T	101.2	HR	88	RR	14	BP	147/71	O2	100% RA
Gen:	Obese male, pleasant and in no acute distress, lying in bed with right foot raised.
HEENT:	PERRL, EOMI, dry mucous membranes.
CV:	RRR, normal S1/S2, no extra heart sounds, no murmurs.
Lungs:	CTAB
Abd:	+BS, non-tender.
Ext:	Right lower extremity with 8x8cm area of erythema predominantly involving lateral aspect of foot, dorsum of foot and 3-5th digits. There is a shallow, 1x1cm ulcer on the plantar surface of foot near 5th MTP. Area is also notable for ecchymosis and palpable crepitus. There is minimal tenderness to palpation or with active/passive range of motion.
Skin:	The remainder of the skin exam is unremarkable.
Neuro:	AAOx3.

Labs/Studies:

BMP: 134/4.3/104/26/18/1.4/206
WBC: 27.3/13.1/40/189 (90% neutrophils)
Lactate: 1.2
CRP: [pending]

Imaging:

CT Lower Extremity

Calf cellulitis and gas-producing cellulitis in the lateral foot and toes.
Thigh and inguinal lymphadenopathy.
Although gas is seen down to the level of the bone, no definite bony changes are identified to establish a diagnosis of osteomyelitis. Please note that MRI is more sensitive for detection of early osteomyelitis.

Assessment/Plan:

40M with DM and diabetic foot ulcer resulting in a necrotizing soft tissue infection as evidenced by gas on imaging. Recommended surgical debridement and started on broad-spectrum antibiotics including:

vancomycin 1g i.v. q.12.h.
cefepime 2g i.v. q.8.h.
metronidazole 500mg i.v. q.8.h.

The patient underwent amputation of 3-5th digits with good surgical margins and was discharged on post-operative day three in good condition.

Skin and soft-tissue layers and their infections: ¹

Necrotizing Soft-Tissue Infections (NSTI):^2,3,4

Risk Factors

IVDA
Comorbid conditions
- DM
- Obesity
- Immunosuppression

Physical Exam

Early (non-specific)
- Swelling
- Erythema
- Pain
Late (non-sensitive)
- Tense edema outside affected skin perimeter
- Disproportionate pain
- Ecchymosis
- Bullae
- Crepitus
- Systemic signs (fever, tachycardia, hypotension)

Treatment

Surgical debridement
Antimicrobials
- Carbapenem, combination B-lactam B-lactamase
- Vancomycin, linezolid (MRSA coverage)
- Clindamycin (inhibit protein synthesis)
Supportive therapy

LRINEC score ⁵

Name	Value	Score
CRP	≥150	4
WBC	15-25 >25	1 2
Hb	11-13.5 <11	1 2
Na	<135	2
Creatinine	>1.6	2
Glucose	>180	1

<5 Low risk, 6-7 Intermediate risk, >8 High risk

References:

Morchi, R. (2/18/14). Emergency Medicine Procedures Cadaver Lab. Clinical Clerkship at UCLA. Los Angeles, CA.
Goldstein, E. J. C., Anaya, D. A., & Dellinger, E. P. (2007). Necrotizing Soft-Tissue Infection: Diagnosis and Management. Clinical infectious diseases, 44(5), 705–710. doi:10.1086/511638
Headley, A. J. (2003). Necrotizing soft tissue infections: a primary care review. American family physician, 68(2), 323–328.
McHenry, C. R., Piotrowski, J. J., Petrinic, D., & Malangoni, M. A. (1995). Determinants of mortality for necrotizing soft-tissue infections. Annals of surgery, 221(5), 558–63.
Wong, C.-H., Khin, L.-W., Heng, K.-S., Tan, K.-C., & Low, C.-O. (2004). The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: A tool for distinguishing necrotizing fasciitis from other soft tissue infections. Critical Care Medicine, 32(7), 1535–1541. doi:10.1097/01.CCM.0000129486.35458.7D

Acute Respiratory Distress Syndrome

HPI:

25M with a history of mild asthma transferred from an outside hospital after 10 days in the intensive care unit for continued management of ARDS.

The patient was well until one week prior to admission when he developed intermittent subjective fevers and general malaise associated with a non-productive cough and nausea/vomiting. He presented to the emergency department of an outside hospital with difficulty breathing and was noted to have respiratory distress and was subsequently admitted. Initial CT at the outside hospital revealed pneumomediastinum but no evidence of pulmonary embolism. Results from the outside hospital reveal a wide array of bacterial/fungal cultures and viral serologies including bronchoscopy but no obvious infectious source. The patient was treated with broad spectrum antibiotics for several days but his condition worsened requiring intubation, mechanical ventilation and transfer to the ICU. Further imaging was suggestive of ARDS, and the patient was transferred for additional management.

The patient was well until one week prior to admission when he reported development of malaise and fatigue. On the day of hospitalization, the patient presented to primary care doctor with complaint of cough and shortness of breath and was found to be in respiratory distress and was admitted. The patient received IV antibiotics (cefepime, vancomycin) and was intubated when respiratory distress worsened. Found to have evidence of ARDS on CXR.

PMH:

Mild asthma, not requiring medication
MRSA skin abscess

PSH:

None

FH:

Non-contributory.

SHx:

Lives with family and works at a local supermarket. Rare alcohol use and no prior tobacco or drug use.
No recent travel or sick contacts.

Meds:

ciprofloxacin 400mg i.v. q12h
linezolid 600mg i.v. q12h
meropenem 1g i.v. q8h
heparin 5000units s.q. q8h
cisatracurium 1.48mcg/kg/min
fentanyl 125mcg/hr
midazolam 10mg/hr
propofol 20mcg/kg/min

Allergies:

NKDA

Physical Exam:

VS:	T	97.8	HR	120	RR	35	BP	123/68	O2	96%
Vent:	PRVC, VT 320, RR 35, PEEP 6, FiO2 95%
Gen:	Young male, thin-appearing, intubated and sedated and not responding to verbal commands
HEENT:	PERRL, unable to assess EOM, ET tube in place
CV:	RRR, normal S1/S2, no murmurs
Lungs:	Coarse breath sounds bilaterally
Abd:	Normoactive bowel sounds, soft, non-distended, no hepatosplenomegaly
Ext:	No clubbing, cyanosis, edema
Neuro:	Unable to assess

Labs/Studies:

CBC: 25.06/7.0/21.3/426
BMP: 132/3.3/88/32/18/1.1/103
ABG: 7.30/97/76/18
Blood/sputum/urine cultures: Negative
Aspergillus, crypto, cocci: Negative
EBV, HIV, influenza, RSV: Negative

Imaging

CT Chest: Evidence of pneumomediastinum and pneumopericardium. Bilateral pulmonary infiltrates, but no pulmonary embolism.

Assessment/Plan:

25M with ARDS transferred from outside hospital for further management.
# ARDS: Severe (P/F ratio <100). Etiology unclear, thorough infectious workup without obvious source. Consider autoimmune or allergic cause.

Ventilator: PRVC lung-protective ventilation
Consider NMB for dyssynchrony despite sedation
Monitor strict I/O, maintain net negative fluid balance.

# Sepsis: Leukocytosis, tachycardia. Continue broad-spectrum antibiotics and monitor cultures.
# Acidosis: Largely respiratory, place dialysis catheter if acute need arises.
# Pneumomediastinum: Possible Boerhaave syndrome given reports of nausea/vomiting.

Pathophysiology of Acute Respiratory Distress Syndrome (ARDS):¹

ARDS represents a stereotyped response to multiple insults. It is characterized by damaged capillary endothelium and alveolar epithelium resulting in increased permeability and the accumulation of fluid in the alveolar space. This causes diffuse alveolar damage and triggers the release of various cytokines (TNF, IL-1, IL-6) which recruit and activate neutrophils causing oxidative cell damage.

Definition of ARDS (Berlin):^2,3

Timing	Acute in onset (<1 week)
Chest imaging	Bilateral opacities
Origin of pulmonary edema	Not explained by heart failure or fluid overload (assessed with echocardiography)
Oxygenation (PaO2/FiO2)	Mild: 200-300 Moderate: 100-200 Severe: <100

Causes of ARDS:^2,4

An Introduction to Mechanical Ventilation:^5,6,7

This is a simplification of the general principles underlying the most common ventilator modes. For more detail, see the articles cited in the references.

Breath Sequences:

Continuous Mandatory Ventilation (CMV)

All breaths controlled by ventilator, no triggered breaths.

Assist-Control Ventilation (AC)

Every patient-triggered breath is fully supported, a backup rate is set. In the absence of patient-triggered breaths, AC acts like CMV.

Synchronized Intermittent Mandatory Ventilation (SIMV)

Preset minimum mandatory breaths are “synchronized” to patient’s efforts. The patient is allowed to breathe spontaneously between supported breaths.

Pressure Support (PS)

All breaths are triggered by the patient and each is supported by preset pressure.

Continuous Positive Airway Pressure (CPAP)

Spontaneous breathing at elevated baseline pressure.

Control Variables:

Volume Control (VC)

Volume is set, pressure is variable. With a drop in compliance, the preset minimum volume is maintained with an increase in pressure.

Pressure Control (PC)

Pressure is set, volume is variable. With a drop in compliance, a smaller volume is delivered to maintain pressures at the preset limit.

Pressure-Regulated Volume Control (PRVC)

Pressure is targeted with a set minimum volume. The ventilator makes breath-to-breath adjustments of pressure to maintain minimum volumes. Breath mechanics are therefore comparable to pressure-control as a defined pressure is delivered based on prior breath’s respiratory mechanics (note pressure and flow tracings for PRVC/PC vs. VC)

References:

Pierrakos C, Karanikolas M, Scolletta S, Karamouzos V, Velissaris D. Acute respiratory distress syndrome: pathophysiology and therapeutic options. J Clin Med Res. 2012;4(1):7–16. doi:10.4021/jocmr761w.
Fanelli V, Vlachou A, Ghannadian S, Simonetti U, Slutsky AS, Zhang H. Acute respiratory distress syndrome: new definition, current and future therapeutic options. J Thorac Dis. 2013;5(3):326–334. doi:10.3978/j.issn.2072-1439.2013.04.05.
ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin Definition. In: Vol 307. 2012:2526–2533. doi:10.1001/jama.2012.5669.
Ware LB, Matthay MA. The acute respiratory distress syndrome. N. Engl. J. Med. 2000;342(18):1334–1349. doi:10.1056/NEJM200005043421806.
Deng, J. (10/20/13). Principles of Mechanical Ventilation. Medical Intensive Care Unit Lecture. Los Angeles, CA.
Singer BD, Corbridge TC. Basic invasive mechanical ventilation. South. Med. J. 2009;102(12):1238–1245. doi:10.1097/SMJ.0b013e3181bfac4f.
Hamed HMF, Ibrahim HG, Khater YH, Aziz ES. Ventilation and ventilators in the ICU: What every intensivist must know. Current Anaesthesia & Critical Care. 2006;17(1-2):77–83. doi:10.1016/j.cacc.2006.07.008.

Cervical Lymphadenopathy

32 year-old male, previously healthy, with slowly-progressive right and left cervical lymphadenopathy over the past three years. He first noted the development of a mass on the lateral neck below the ear three years ago. This mass was non-tender and remained stable at approximately the size of a marble for nearly one year. He later developed more and larger masses, but never experienced any constitutional symptoms like fevers, night sweats, fatigue or weight loss. Examination reveals a healthy, well-nourished male with multiple, hard, mobile, non-tender right posterior cervical and submandibular lymph nodes and a large left supraclavicular lymph node, protruding above the clavicle and measuring ~4x3cm.

Imaging:

Cervical Lymphadenopathy - Axial

- Left supra-clavicular lymph node, 4.5 x 2.9 cm
- Right posterior submandibular lymph node, 3.5 x 2.7 cm
- Multiple other small cervical lymph nodes, more on the right

Cervical Lymphadenopathy - Coronal

- Left supra-clavicular lymph node, 4.5 x 2.9 cm
- Right posterior submandibular lymph node, 3.5 x 2.7 cm
- Multiple other small cervical lymph nodes, more on the right

He has undergone several diagnostic procedures during this time including aspirations and core biopsies with inconclusive pathology and he is currently admitted for an excisional biopsy of the supraclavicular lymph node. Infectious and rheumatologic workup has remained negative including: HIV, bartonella, Quantiferon TB Gold, cocci, histo, toxo, CMV, EBV, ANA, RF, ACE.

The patient tolerated the excisional biopsy without complication and was discharged. Preliminary pathology suggests Castleman’s disease.

Lymph nodes and their drainage: ^1,2

Evaluation of Lymphadenopathy: ^2,3,4

References:

Ferrer R. Lymphadenopathy: differential diagnosis and evaluation. Am Fam Physician. 1998;58(6):1313–1320.
Henry PH, Longo DL. Chapter 59. Enlargement of Lymph Nodes and Spleen. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 18e. New York: McGraw-Hill; 2012.
Armitage JO. Chapter 171. Approach to the Patient With Lymphadenopathy and Splenomegaly In: Cecil, Russell L., Lee Goldman, and Andrew I. Schafer. Goldman’s Cecil medicine. Philadelphia: Elsevier/Saunders, 2011.
Motyckova G, Steensma DP. Why does my patient have lymphadenopathy or splenomegaly? Hematol. Oncol. Clin. North Am. 2012;26(2):395–408– ix. doi:10.1016/j.hoc.2012.02.005.

Hepatic Abscess

HPI:

42M with 1.5 weeks of fevers. Initially presented to ER 1wk ago and treated for possible otitis media, however follow-up ENT appointment showed no evidence of OM on exam. Fevers persisted and he developed headaches and went to urgent care where a CT head and LP were negative. A mild elevation of serum transaminases was noted and the following CT abdomen/pelvis was obtained. He denied GI symptoms.

Imaging:

Hepatic Abscess - Axial

- 7.4 cm cystic lesion in the inferior right lobe of the liver most consistent in appearance with hepatic abscess.
- Multiple calcified gallstones with a 10 mm gallstone in the neck of the gallbladder or possibly in the cystic duct.

Hepatic Abscess - Coronal

Assessment & Plan:

# Liver abscess: likely pyogenic s/p CT-guided drainage with 60cc purulent fluid removed. Gram stain showed GNR and WBC’s, culture grew Klebsiella pneumonia. Treated with ceftriaxone 2g IV q24h, metronidazole 500mg PO TID.

Differential Diagnosis of Hepatic Abscess:¹

References:

Krige J, Beckingham IJ. Liver abscesses and hydatid disease. BMJ. 2001;322(7285):537–540.

Volvulus

Swirling mesenteric vessels in mid-pelvis associated with narrowed segments of small bowel and fluid-filled proximal small bowel raises concern for volvulus and small bowel obstruction.

Alcoholic Hepatitis

HPI:

43 year-old female with a history of alcohol abuse and alcoholic hepatitis, presenting after referral from breast clinic for abnormal labs (notable for total bilirubin 18.1). The patient was well until two weeks ago when she noted increasing fatigue associated with morning nausea/vomiting (non-bloody) as well as yellowing of skin and eyes. She also reports darkening of urine, but no dysuria, change in volume of urine, or visible blood. She also denies fevers/chills, increased abdominal girth, abdominal pain, changes in bowel habits or bloody/dark stools.

She reports drinking 1 pint of vodka daily for the past 15 years, and perhaps more in the past 3 weeks. Her last drink was in the morning on the day of admission, she denies any history of seizures and reports withdrawal symptoms (tremor, nausea) relieved with more alcohol. She currently denies anxiety/agitation, tactile/visual/auditory hallucinations.

The patient was in breast clinic for evaluation of a painful breast mass which developed after biopsy of a lesion which was ultimately found to be benign. The patient noted the mass was growing in size and becoming more painful over the past month.

PMH:

EtOH abuse
Alcoholic hepatitis

PSH:

None

FH:

No family history of breast/gynecologic malignancy.
Mother with history of stroke. Father with diabetes.

SHx:

Lives alone.
Denies current or previous tobacco/drug use. Drinks 1 pint of whiskey daily for the past 15 years.
Not currently sexually active, no history of STI.

Meds:

None

Allergies:

NKDA

Physical Exam:

VS:	T	98.9	HR	104	RR	19	BP	117/67	O2	99% RA
Gen:	Well-appearing obese female in no acute distress
HEENT:	PERRL, marked scleral icterus, sublingual icterus, MMM, no lesions
CV:	Tachycardia, regular rhythm, normal S1/S2, no M/R/G
Lungs:	CTAB, no crackles/wheezing
Abd:	+BS, soft, non-distended, liver edge palpated 6cm below costal margin, irregular texture slightly tender to palpation, spleen not palpated, no fluid wave or shifting dullness, no rebound/guarding.
Ext:	Warm, well-perfused, 2+ pulses (DP/PT), slight yellowing.
Skin:	Vascular spiders on anterior chest, left breast with 5x5cm ecchymosis and tender underlying mass, no erythema, warmth, skin dimpling, nipple discharge.
Neuro:	AAOx4, CN II-XII intact, no tremor noted, gait normal.

Labs/Studies:

1mo prior to admission:

AST/ALT/AP/TB: 444/77/234/2.5

Day 1:

AST/ALT/AP/TB: 185/61/184/18.1
PT/PTT/INR: 14.7/37.0/1.2

Day 4:

AST/ALT/AP/TB: 142/50/153/25.5
PT/PTT/INR: 20.1/38.9/1.7

Imaging:

Abdominal US

Markedly echogenic and enlarged liver with a nodular surface of cirrhosis.
Markedly blunted hepatic vein waveforms commonly seen due to decreased hepatic parenchymal compliance although other etiologies causes of obstruction to hepatic venous outflow.
Splenomegaly.

Assessment/Plan:

44F hx EtOH abuse, alcoholic hepatitis, presenting with acute alcoholic hepatitis.
# Alcoholic hepatitis: Rapid onset of jaundice, tender hepatomegaly, and elevation of transaminases (AST > ALTx2) in the setting of chronic alcohol use suggestive of alcoholic hepatitis. Initial Maddrey discriminant hepatic function (mDH) score 37 suggestive of severe disease with high short-term mortality. Initiated trental 400mg p.o. t.i.d.
# EtOH withdrawal: Last drink <24h ago, monitor for signs of withdrawal, treat with Ativan per withdrawal protocol. # Cirrhosis: Newly diagnosed on abdominal ultrasound. Complicated by coagulopathy, and likely portal hypertension given splenomegaly/thrombocytopenia. Plan for outpatient screening EGD and continued GI follow-up. # Breast mass: Likely hematoma 2/2 biopsy associated given increased size associated with progression of coagulopathy/thrombocytopenia. Outpatient ultrasound and follow-up scheduled. # Anemia: Macrocytic, potentially related to vitamin deficiency vs. bone-marrow suppression associated with chronic alcohol use. Start thiamine/folate/multivitamin. # FEN/GI/PPx: Encourage p.o. intake (2g sodium restriction), continue ondansetron p.r.n. nausea/vomiting, obtain nutrition consult.

Hospital Course

Patient’s liver function continued to decline as evidenced by worsening coagulopathy and increased serum bilirubin. mDH had increased to 58 by day four of hospitalization and steroids were added.

Pathophysiology of Alcoholic Hepatitis: ¹

Ethanol promotes translocation of bacterial components (lipopolysaccharide) across the intestinal wall, into the portal venous system and liver. These trigger a local and systemic inflammatory response which leads to hepatocellular injury and systemic effects such as fever, anorexia and weight loss.

Evaluation of Alcoholic Hepatitis: ^1,2

Clinical features:

Rapid onset jaundice
Tender hepatomegaly
Fever
Ascites
Proximal muscle loss
Encephalopathy

Labs:

AST > ALT (x2), generally < 300IU/mL
Leukocytosis
↑Total serum bilirubin
↑INR
↑Creatinine associated with poor prognosis

Other studies:

Screening for infection: PNA, UTI, SBP
Abdominal US to evaluate hepatic abscess, HCC, extrahepatic biliary obstruction

Management of Alcoholic Hepatitis: ^1,2

Grading Severity:

Maddrey’s discriminant function
Glasgow score
Lille score (assess response to corticosteroids after 1wk)

Treatment:

Immediate and lifetime abstinence from alcohol
Trental 400mg p.o. t.i.d.
Prednisolone 40mg p.o. daily (controversial, some benefit in subgroup with Maddrey > 32)
Ascites: Sodium restriction, diuretics
Encephalopathy: Lactulose, rifaximin
Hepatorenal syndrome: albumin, vasopressors
Nutritional support

Interpretation of Liver Function Tests: ³

Disorder	Bilirubin	AST/ALT	AΦ	Albumin	PT
Hemolysis Gilbert	↑(indirect) No bilirubinuria	–	–	–	–
Acute hepatocellular necrosis	↑	↑ALT > AST > 500IU	↑	–	– (poor prognosis if elevated)
Chronic liver disease	↑	↑ < 300IU	↑	↓	↑
Alcoholic hepatitis	↑	↑ AST:ALT > 2	↑	↓	↑
Intra- extra-hepatic cholestasis	↑	↑ < 500IU	↑↑ (>4x normal)	–	–

Features of Components of Liver Function Tests: ^3,4

References:

Lucey, M. R., Mathurin, P., & Morgan, T. R. (2009). Alcoholic hepatitis. The New England journal of medicine, 360(26), 2758–2769. doi:10.1056/NEJMra0805786
Sohail, U., & Satapathy, S. K. (2012). Diagnosis and management of alcoholic hepatitis. Clinics in liver disease, 16(4), 717–736. doi:10.1016/j.cld.2012.08.005
Kaplan MM. Chapter 302. Evaluation of Liver Function. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012.
Johnston, D. E. (1999). Special considerations in interpreting liver function tests. American family physician, 59(8), 2223–2230.

Head Trauma: Radiographic Evolution

CT Head (Initial)

- Noncontrast axial images through the head demonstrate no evidence of skull fracture.
- Large lentiform-shaped mixed density extra-axial acute epidural hematoma in the right parietal occipital
- Associated subdural hematoma tracking along right convexity toward the right temporal lobe.
- There is no evidence of midline shift.

CT Head (+8h)

- Significant interval increase in the size of the right hemispheric subdural hematoma
- There is now midline shift from right to left at the level of the septum pellucidum measuring 10 mm, partial effacement of the right lateral ventricle and subfalcial herniation.
- Scattered subarachnoid blood is redemonstrated.
- Comminuted fractures of the nasal bone are present and there is overlying and associated periorbital soft tissue swelling.

CT Head (+16h, s/p SDH evacuation)

- Interval gross total evacuation of right hemispheric subdural hematoma.
- Moderate anterior bifrontal subdural and right epidural air is present.
- Small scattered subarachnoid and intraventricular blood is redemonstrated.

Joint Pain and Tremor

HPI:

47 year-old female with a history of arthritis, gout and AVP (5/2013) resulting in tib/fib fracture s/p ORIF presenting with severe joint pain, worsening in the past week such that she has been unable to walk. While she reported significant diffuse joint pain, it was predominantly focused on her left leg, bilateral knees, and left shoulder. Joint pain progressively worsens over the course of the day and is worse with activity (better at rest). She reported occasional joint swelling, but no redness, fevers/chills, new trauma, recent travel, and is not sexually active. She reports suffering from joint pain for over 10 years, previously well-controlled with OTC pain medications (ibuprofen), however this had grown ineffective in the past week. She had been prescribed Norco after her surgery but was unable to afford it. She denies any recent intake of foods that have previously been triggers for acute gouty flares.

PMH:

Arthritis
Gout

PSH:

Left tib/fib fracture s/p ORIF

FH:

No family history of RA, SLE or joint disease.

SHx:

No t/e/d use
Lives at home alone

Meds:

Ibuprofen 800mg p.o. p.r.n. pain

Allergies:

NKDA

Physical Exam:

VS:	T 98.1 HR 109 RR 18 BP 108/66 O2 95% RA
Gen:	Thin female, appearing older than her stated age, in significant pain when helped to transfer to bed for examination
HEENT:	PERRL, MMM, no lesions
CV:	RRR, normal S1/S2, no M/R/G
Lungs:	CTAB, no crackles/wheezing
Abd:	+BS, soft, NT/ND, no masses
Ext:	Knees appear symmetric, no deformities, no erythema or warmth to touch, no effusion detected, significant tenderness to light touch of bilateral knees. Significant decreased ROM 2/2 pain in b/l lower extremities, limited to 30 degrees of knee flexion, unable to test strength 2/2 pain.Left lower extremity with 6cm longitudinal incisions on lateral and medial aspects of leg. Incisions appear well-healed without erythema/discharge. Decreased sensation on lateral and medial aspects of left leg. Left shoulder appears normal, no obvious deformities, no bony tenderness. Decreased ROM to 15 degrees of abduction/flexion/extension 2/2 pain.
Neuro:	AAOx4, CN II-XII intact, gait not tested. A high-frequency, high-amplitude tremor is noted in the bilateral upper extremities at rest and with activity. Tremor appears associated with patient’s distress and pain.

Labs/Studies:

CBC: 9.4/12.8/38.1/311
BMP: 135/3.9/100/27/14/0.60/113
CRP: 0.18
ESRW: 20
Uric Acid: 2.6
XR Left Tibia/Fibula: There is a metallic fixation device noted in the tibia. There is no evidence of loosening of the metallic components. The bones appear to be in gross anatomic alignment.

Assessment/Plan:

47F w/hx arthritis, gout, recent tib/fib fx s/p ORIF presenting with worsening polyarticular arthralgia unresponsive to OTC medications admitted for evaluation and pain management.

# Polyarticular arthralgia: Multiple joints affected, however patient notes most significant in bilateral knees and recently operated left leg. Polyarticular involvement, symmetric distribution and predominant involvement of large joints is suggestive of osteoarthritis. Also, given patient’s significant distress and multiple points of tenderness, potential extra-articular cause such as complex regional pain syndrome. Unlikely inflammatory arthritis (infectious, crystal arthropathy, rheumatic disease) given distribution and no significant erythema, warmth or effusion which could be aspirated. Obtained imaging of LLE to evaluate recent surgical repair of tib/fib fracture, with no evidence of loosening of fixation components or misalignment. Patient’s symptoms improved with morphine 5mg i.v. x2 in ED. Will admit for continued evaluation and pain management, consider addition of gabapentin for potential neuropathic pain associated with recent surgery.

# Tremor: High-frequency, high-amplitude rest and action tremor suggestive of essential tremor or exaggerated physiological tremor associated with pain and emotional distress. No other neurological symptoms (HA, weakness) and non-focal neurological exam (aside from anesthesia localized around recent surgical incisions in LLE). Will continue monitoring, no need for imaging at this time.

# Gout: Patient with history of gout, however, doubt that current arthralgia associated with acute gouty flare. Will continue monitoring exam and consider ortho consultation for joint aspiration.

Differential Diagnosis of Monoarticular Arthralgia: ^1,2

Differential Diagnosis of Polyarticular Arthralgia ^1,3

Use of Serum Uric Acid in Acute Gout ⁴

In this patient, serum uric acid levels were checked. However, a normal serum urate (SU) does not exclude an acute gout flare. Studies have shown 12-43% of patients with acute gout flares have normal SU. An elevated SU (>8.0mg/dL) may support the diagnosis of a gout flare but is not itself diagnostic.

Approach to Joint Pain: ³

Approach to Joint Pain

Certain key historical elements can help narrow the differential diagnosis.

Inflammation:
1. Definition: Presence of erythema, warmth, swelling, pain with passive ROM, morning stiffness suggests inflammatory cause (arthritis)
2. Common causes: Infection, gout, RA, SLE
Chronology:
1. Definition: Acute <6wks, chronic > 6wks
Distribution:
1. Definition: Location (large/small), symmetry
2. Common causes:
  1. OA: DIP + PIP, spares wrists, elbows, ankles
  2. RA: PIP + MCP
  3. Spondylarthropathies (large joints)
  4. Symmetric involvement: RA, SLE
  5. Asymmetric involvement: Psoriatic arthritis, reactive arthritis, gout
Course:
1. Definition: Intermittent (gout), migrating (GC, Lyme, SLE)
Demographics:
1. Female <50: RA, SLE
2. Male > 40: gout (♂ 20yr after puberty, ♀ 20yr after menopause)
Extra-articular manifestations:
1. Malar rash, oral ulcers: SLE
2. Proximal muscle weakness: polymyositis
3. Psoriatic skin/nail lesions: psoriatic arthritis
4. Oral ulcers, vesicopustules on palms/soles, recent diarrheal illness: reactive arthritis

Differential Diagnosis of Tremor: ^5,6

References:

Cush JJ, Lipsky PE. Chapter 331. Approach to Articular and Musculoskeletal Disorders. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. http://www.accessmedicine.com/content.aspx?aID=9139045. Accessed August 27, 2013.
Siva, C., Velazquez, C., Mody, A., & Brasington, R. (2003). Diagnosing acute monoarthritis in adults: a practical approach for the family physician. American family physician, 68(1), 83–90.
Mies Richie, A., & Francis, M. L. (2003). Diagnostic approach to polyarticular joint pain. American family physician, 68(6), 1151–1160.
Schlesinger, N., Norquist, J. M., & Watson, D. J. (2009). Serum urate during acute gout. The Journal of rheumatology, 36(6), 1287–1289. doi:10.3899/jrheum.080938
Hess, C. W., & Pullman, S. L. (2012). Tremor: clinical phenomenology and assessment techniques. Tremor and other hyperkinetic movements (New York, N.Y.).
Crawford, P., & Zimmerman, E. E. (2011). Differentiation and diagnosis of tremor. American family physician, 83(6), 697–702.

Hyperglycemic Crises

CC:

Blurred vision, numbness

HPI:

56 year-old male with a history of DM, questionable HTN presenting with blurred vision, numbness of fingertips/toes for 2wks. Associated symptoms include dry mouth, polydipsia/polyuria. He states that these symptoms coincide with elevated measurements of blood glucose at home (>500). He ran out of his diabetes medication (metformin) 8mo ago but states his BG was typically between 100-200 with diet/exercise until 2wks ago. He reports recent dietary indiscretions on a trip to Las Vegas.

He denies fevers/chills, CP/SOB, cough, abdominal pain, N/V, or dysuria.

PMH:

DM II
HTN

PSH:

None

FH:

Several maternal family members with DM.

SHx:

No tobacco/drug use
5-6 alcoholic drinks/wk

Meds:

Metformin 500mg p.o. b.i.d.

Allergies:

NKDA

Physical Exam:

VS:	T 37.8 HR 60 RR 14 BP 165/90 O2 99% RA
Gen:	Well-appearing, no acute distress, obese
HEENT:	PERRL, EOMI, optic discs sharp b/l, no abnormalities visualized
CV:	RRR, normal S1/S2, no M/R/G, no additional heart sounds
Lungs:	CTAB, no wheezes/crackles
Abd:	+BS, soft, NT/ND, no rebound/guarding
Ext:	Warm, well-perfused, 2+ pulses, no clubbing/cyanosis/edema
Neuro:	AAOx3, CN II-XII intact

Labs/Studies:

BMP: 135/3.8/102/24/18/1.1/378
CBC: 7.4/14.1/42.0/403
UA: + glucose, – ketones

Assessment/Plan:

56M, hx DM with poor medication adherence presenting with vision changes and stocking/glove paresthesias for 2wks after reported dietary indiscretion found to be hyperglycemic. DKA/HHS unlikely given stable vital signs, normal metabolic panel with exception of isolated hyperglycemia (slight hyponatremia likely related to osmotic effect of elevated serum glucose). Also, no evidence of concerning precipitates for hyperglycemic crisis (no CP/SOB, no F/C, no cough, no abdominal pain, no change in mental status). Patient was discharged home with education on importance of medication adherence, refill of metformin, and follow-up with primary care physician for further management of DM and possible hypertension.

Evaluation of hyperglycemic crises in patients with diabetes:^1,2

Key signs/symptoms of HHS/DKA:

Both: Polyuria, polydipsia, weight loss, hypovolemia (dry MM, skin turgor, tachycardia, hypotension)
DKA: Short course (<24h), N/V, diffuse abdominal pain, Kussmaul respirations
HHS: Longer course (days/weeks), altered mental status (lethargy, coma, seizure)

Admission Laboratory Data of Patients with HHS vs. DKA:¹

	DKA	HHS
Glucose (mg/dl)	616	930
pH	7.12	7.30
3-β-hydroxybutyrate (mmol/l)	9.1	1.0
Serum osmolality	323	380
Delta gap (AG-12)	17	11
Na (mEq/l)	134	149
K (mEq/l)	4.5	3.9
Bicarbonate (mEq/l)	9	18

References:

Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes care, 32(7), 1335–1343. doi:10.2337/dc09-9032
De Beer, K., Michael, S., Thacker, M., Wynne, E., Pattni, C., Gomm, M., Ball, C., et al. (2008). Diabetic ketoacidosis and hyperglycaemic hyperosmolar syndrome – clinical guidelines. Nursing in critical care, 13(1), 5–11. doi:10.1111/j.1478-5153.2007.00259.x
Stoner, G. D. (2005). Hyperosmolar hyperglycemic state. American family physician, 71(9), 1723–1730.

Angioedema

HPI:

63-year old African American male with a history of HTN presenting with lip swelling x1 day. The patient states he was well until this morning when he noticed progressive swelling of his lips. The swelling is not associated with any difficulty speaking, swallowing or breathing and is not painful.

He denies new rashes or itching, and has no history of such swelling. He also denies any exposure to known allergens, recent insect bites or travel. He has been taking lisinopril for his blood pressure regularly for the past several months and denies any prior adverse effects (cough, rash).

PMH:

Parkinson Disease
HTN

PSH:

None

FH:

No family history of angioedema

SHx:

No t/e/d use
Lives at home with caretaker

Meds:

Lisinopril 20mg p.o. daily
Carbidopa/levodopa 50mg p.o. t.i.d.

Allergies:

NKDA

Physical Exam:

VS:	T 37.8 HR 84 RR 14 BP 146/98 O2 99% RA
Gen:	Well-appearing, no respiratory distress, speaking comfortably
HEENT:	PERRL, significant external upper/lower lips swelling extending to lateral cheeks, non-tender, no fluctuance or overlying skin changes. No visible tongue swelling, floor of mouth swelling/tenderness, uvular/palatal deviation.
CV:	RRR, no M/R/G
Lungs:	CTAB, no crackles/wheezing, good air movement b/l
Abd:	+BS, soft, NT/ND, no rebound/guarding
Ext:	Warm, well-perfused, 2+ peripheral pulses
Skin:	No visible skin lesions/rashes
Neuro:	AAOx4, CN II-XII intact

Assessment/Plan:

63M with acute onset, progressive facial swelling. Currently restricted to external lips, with no evidence of airway compromise. Likely ACE inhibitor-induced angioedema given patient is on lisinopril and has no history of hereditary angioedema. Doubt anaphylaxis given no allergies, suspicious exposures or history of pruritus. Doubt infection given afebrile and painless swelling without e/o erythema.

Pathophysiology of ACE inhibitor-induced angioedema¹

Angioedema is a vascular reaction associated with tissue (subcutaneous, submucosal) edema resulting from increased activity of vasoactive substances. The vasoactive substances in ACE inhibitor-induced angioedema are bradykinin and substance P. In the presence of ACE inhibition, these enzymes are inactivated through alternative pathways which, if disturbed, lead to angioedema.

Epidemiology of ACE inhibitor-induced angioedema

Angioedema occurs in 0.1-0.7% of patients taking ACE inhibitors, and 60% of cases occur within the first week of starting an ACE inhibitor (though it can occur as much as years later).^2,3 ACE inhibitors are implicated as the cause of 20-40% of all ED visits for angioedema.⁴

Risk Factors^2,5,6

Female
Age > 65yo
African American
Prior angioedema
Smoking
ACE inhibitor-associated cough

Clinical Features of ACE inhibitor-induced angioedema

Affected Sites:

Mucous membranes of the head and neck
- Face
- Tongue
- Lips
- Pharynx
- Larynx
GI tract
- Diffuse abdominal pain
- Nausea/vomiting/diarrhea

Signs/Symptoms at initial presentation:⁴

SOB (89%)
Lip swelling (70%)
Tongue swelling (52%)
Voice change/hoarseness (29%)
Stridor (11%)

Key Clinical Features:

Onset in minutes with resolution in 24-72 hours
Absence of itching/urticaria⁷

Staging and Disposition:⁸

Stage	Affected Site	Outpatient (%)	Floor (%)	ICU (%)	Intervention (%)
I	Face, lip	48	52	0	0
II	Soft palate	60	40	0	0
III	Tongue	26	7	67	7
IV	Larynx	0	0	100	24

Management of ACE inhibitor-induced angioedema

Proven benefit
- Airway management
- Withdrawal of ACE inhibitor
Unclear benefit
- Epinephrine 0.3mg IM q15min
- Diphenhydramine 50mg IV
- Famotidine 20mg IV
- Solumedrol 125mg IV
Future treatment options
- FFP: contains ACE⁹
- Icatibant: bradykinin B2 receptor antagonist^10,11

References:

Vleeming, W., van Amsterdam, J. G., Stricker, B. H. C., & de Wildt, D. J. (1998). ACE inhibitor-induced angioedema. Drug Safety, 18(3), 171–188. doi:10.2165/00002018-199818030-00003
Grant, N. N., Deeb, Z. E., & Chia, S. H. (2007). Clinical experience with angiotensin-converting enzyme inhibitor-induced angioedema. Otolaryngology – head and neck surgery, 137(6), 931–935. doi:10.1016/j.otohns.2007.08.012
Slater, E. E., Merrill, D. D., Guess, H. A., Roylance, P. J., Cooper, W. D., Inman, W. H., & Ewan, P. W. (1988). Clinical profile of angioedema associated with angiotensin converting-enzyme inhibition. JAMA : the journal of the American Medical Association, 260(7), 967–970.
Banerji, A., Clark, S., Blanda, M., LoVecchio, F., Snyder, B., & Camargo, C. A. (2008). Multicenter study of patients with angiotensin-converting enzyme inhibitor-induced angioedema who present to the emergency department. Annals of allergy, asthma & immunology, 100(4), 327–332. doi:10.1016/S1081-1206(10)60594-7
Gibbs, C. R., Lip, G. Y., & Beevers, D. G. (1999). Angioedema due to ACE inhibitors: increased risk in patients of African origin. British journal of clinical pharmacology, 48(6), 861–865.
Morimoto, T., Gandhi, T. K., Fiskio, J. M., Seger, A. C., So, J. W., Cook, E. F., Fukui, T., et al. (2004). An evaluation of risk factors for adverse drug events associated with angiotensin-converting enzyme inhibitors. Journal of evaluation in clinical practice, 10(4), 499–509. doi:10.1111/j.1365-2753.2003.00484.x
Kanani, A., Schellenberg, R., & Warrington, R. (2011). Urticaria and angioedema. Allergy, Asthma & Clinical Immunology, 7(Suppl 1), S9. doi:10.1186/1710-1492-7-S1-S9
Ishoo, E., Shah, U. K., Grillone, G. A., Stram, J. R., & Fuleihan, N. S. (1999). Predicting airway risk in angioedema: staging system based on presentation. Otolaryngology – head and neck surgery, 121(3), 263–268.
Hassen, G. W., Kalantari, H., Parraga, M., Chirurgi, R., Meletiche, C., Chan, C., Ciarlo, J., et al. (2013). Fresh frozen plasma for progressive and refractory angiotensin-converting enzyme inhibitor-induced angioedema. The Journal of emergency medicine, 44(4), 764–772. doi:10.1016/j.jemermed.2012.07.055
Bas, M., Greve, J., Stelter, K., Bier, H., Stark, T., Hoffmann, T. K., & Kojda, G. (2010). Therapeutic Efficacy of Icatibant in Angioedema Induced by Angiotensin-Converting Enzyme Inhibitors: A Case Series. Annals of emergency medicine, 56(3), 278–282. doi:10.1016/j.annemergmed.2010.03.032
MD, M. G., & MD, M. A. (2012). Icatibant: a novel approach to the treatment of angioedema related to the use of angiotensin-converting enzyme inhibitors. American Journal of Emergency Medicine, 30(8), 1664.e1–1664.e2. doi:10.1016/j.ajem.2011.09.014

Hearing loss and Tinnitus

HPI:

42 year-old male with no significant medical history presenting to ENT clinic after referral from PMD for perforated TM. The patient last had normal hearing approximately 1yr ago when he noted acute onset of right ear pain, discharge, hearing loss and ringing in the setting of fever and a productive cough. He does not recall an inciting event (trauma, swimming) to this initial episode, and had no previous history of ear infections. He saw his PMD several days later, was told he had a perforated ear drum and was treated with antibiotics.

Since then, the patient has not had any further ear pain or discharge but is left with persistent and constant hearing loss and ringing (high-pitched, non-pulsatile).

PMH:

None

PSH:

None

FH:

Non-contributory

SHx:

Worked in construction for 20yrs

Meds:

None

Allergies:

NKDA

Physical Exam:

Gen:	Well-appearing, no acute distress
Head:	NC/AT
Eyes:	PERRL (4-2mm), disc margins sharp
Ears:	Weber lateralizes to left, AC > BC b/l AD: Decreased acuity to finger rub, EAC with some cerumen, cleared to reveal central perforation in posterior-superior quadrant of tympanic membrane. AS: EAC clear, TMI
Nose:	Nasal mucosa pink, septum midline
Mouth:	MMM, no lesions, good dentition, no pharyngeal erythema/exudates
Neck:	Trachea midline, supple, no cervical lymphadenopathy, no thyroid enlargement

Studies

Audiogram: Severe low-mid frequency progressing to profound high frequency mixed hearing loss

Assessment/Plan:

42M, no significant PMH, with perforated TM and audiogram showing mixed hearing deficit. The patient describes a history suggestive of acute otitis media complicated by TM perforation. Persistent perforation seen on examination today can result in the tinnitus and hearing loss the patient complains of. However the marked sensorineural component remains unexplained, particularly given the patient reported previously normal hearing. While there is some evidence that acute otitis media can lead to sensorineural hearing loss, it is typically only mild and only in high-frequency ranges.^1,2 Plan for further evaluation with repeat audiogram and MRI IAC, RTC when studies completed.

Examination of the Ear³

External Auditory Canal: in acute otitis externa, the canal will be narrowed, swollen and erythematous
Tympanic Membrane: use cone of light for orientation, identify malleus and move speculum to visualize all four quadrants

Differential Diagnosis of Hearing Loss⁴

Differential Diagnosis of Tinnitus⁵

References:

Tarlow, M. (1998). Otitis media: pathogenesis and medical sequelae. Ear, nose, & throat journal, 77(6 Suppl), 3–6.
Tsuprun, V., Cureoglu, S., Schachern, P. A., Ferrieri, P., Briles, D. E., Paparella, M. M., & Juhn, S. K. (2008). Role of pneumococcal proteins in sensorineural hearing loss due to otitis media. Otology & neurotology, 29(8), 1056–1060.
Bickley, Lynn S., Peter G. Szilagyi, and Barbara Bates. Bates’ guide to physical examination and history taking. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2009. Print.
Isaacson, J. E., & Vora, N. M. (2003). Differential diagnosis and treatment of hearing loss. American family physician, 68(6), 1125–1132.
Crummer, R. W., & Hassan, G. A. (2004). Diagnostic approach to tinnitus. American family physician, 69(1), 120–126.

Dysphonia (Hoarseness)

Case 1

HPI:

36 year-old female with no significant medical history who presents after referral for voice hoarseness. According to the patient, she underwent a C-section 3 months ago (at an outside hospital) complicated by bleeding requiring a second operation (L salpingoophorectomy); however, neither procedure required emergent intubation. She reports that she had some vomiting associated with anesthesia which ultimately required intubation and admission to the MICU for 5-6d. She was discharged 10 days after the initial operation, and both she and her baby were in good health. Two weeks after discharge, she began experiencing throat irritation and 1 month after discharge she noticed voice hoarseness which has been persistent. Today, she denies difficulty swallowing or breathing, F/C, N/V, abdominal pain.

PMH:

None

PSH:

Cesarean x2, L salpingoophorectomy

FH:

Non-contributory

SHx:

Lives at home taking care of 3 children, denies t/e/d

Meds:

None

Allergies:

NKDA

Physical Exam:

Gen:	WA, NAD
Head:	NC/AT
OC:	MMM, no lesions, no pharyngeal erythema/exudates, hoarse voice
Ears:	EAC clear, TMI b/l
Flex:	Posterior commissure edema, cobblestoning, b/l TVC with shiny white masses

Flexible nasolaryngoscopy image showing trauma granulomata.

Assessment/Plan:

36F, no significant PMH, recent Cesarean and L salpingoophorectomy c/b likely aspiration requiring intubation and mechanical ventilation for several days with onset of progressive voice hoarseness 1mo later. History and flexible nasolaryngoscopy consistent with trauma granulomata, as well as laryngopharyngeal reflux.

Discussed treatment options with patient, recommend voice rest x2mo and continued monitoring
Laryngopharyngeal reflux, given dietary/lifestyle education, start omeprazole 20mg p.o. b.i.d.
RTC 1mo

Case 2

HPI:

51 year-old female with a history of Hepatitis C, COPD and an 80 pack-year smoking history presents with concern about progressive voice hoarseness x2mo. She reports quitting smoking two months ago and is not sure if the hoarseness preceded or followed quitting. She has occasional throat discomfort which is mild. She otherwise denies difficulty or pain with swallowing, worsening shortness of breath, unintentional weight loss.

She also reports a new mass on her neck which she first noticed yesterday. Denies associated pain, or surrounding skin changes.

PMH:

Hepatitis C
COPD

PSH:

Hysterectomy

FH:

Non-contributory

SHx:

80 pack-year smoking history, no current EtOH, drug use (previously used heroin and opiates)

Meds:

Methadone
Elavil
Multiple unknown inhaled medications

Allergies:

Naproxen (swelling)

Physical Exam:

Gen:	WA, NAD
Head:	NC/AT
Eyes:	PERRL, EOMI
Ears:	b/l EAC erythema, TMI, no lesions/exudates
OC:	MMM, no lesions
Neck:	Supple, no thyroid enlargement, no cervical lymphadenopathy, 5x6cm soft, round, mobile, non-tender mass on left lateral neck w/o overlying skin changes
Flex:	Diffuse laryngeal damage, thickened posterior commissure, right TVC with area of leukoplakia, left TVC appears irregular

Assessment/Plan:

51F hx HepC, COPD, 80py smoking, presenting with voice hoarseness x2mo. History concerning for malignancy, exam today shows significant laryngeal damage and vocal cord irregularities warranting further evaluation. Possible component of fungal infection 2/2 inhaled steroid use for COPD, plan to reduce potentially aggravating factors (treat fungal infection, voice rest) and repeat evaluation. Neck mass possibly lipoma however will evaluate further given concern for malignancy.

Start fluconazole 100mg two tables p.o. on day1, 100mg p.o. daily x7d
Start nystatin 100,000 units/mL 10mL gargle and swallow t.i.d. x2wks
Advised voice rest
RTC in 3wks
CT neck/soft tissue w/wo IV contrast to evaluate neck mass

Anatomy of the Pharynx/Larynx:

Physiology of Voice Production: ¹

Voice is produced through the passive vibration of vocal folds in an air stream and requires:

Adequate Air Stream
Smooth vocal fold edges
Vocal folds with normal vibratory properties
Appropriate vocal fold positioning

Differential diagnosis of dysphonia (hoarseness): ^1,2,3

Characteristics of Hoarse Voice: ⁵

Characteristic	Likely cause
Breathy	Vocal cord paralysis
Hoarse	Vocal cord lesion, LPR
Low-pitched	Reinke’s edema, vocal abuse, LPR

References:

Mau, T. (2010). Diagnostic Evaluation and Management of Hoarseness. Medical Clinics of North America, 94(5), 945–960. doi:10.1016/j.mcna.2010.05.010
Feierabend, R. H., & Shahram, M. N. (2009). Hoarseness in adults. American family physician, 80(4), 363–370.
Schwartz, S. R., Cohen, S. M., Dailey, S. H., Rosenfeld, R. M., Deutsch, E. S., Gillespie, M. B., Granieri, E., et al. (2009, September). Clinical practice guideline: hoarseness (dysphonia). Otolaryngology. doi:10.1016/j.otohns.2009.06.744
Bruch, J.W., Kamani D.V. Diaphragmatic pacing. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
Rosen, C. A., Anderson, D., & Murry, T. (1998). Evaluating hoarseness: keeping your patient’s voice healthy. American family physician, 57(11), 2775–2782.

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs/Studies:

Imaging:

Assessment/Plan:

Hospital Course:

Differential Diagnosis of Hypocalcemia: 1,2

Laboratory Evaluation of Hypocalcemia: 1,2

Clinical Manifestations of Hypocalcemia: 1

Management of Symptomatic Hypocalcemia: 1

Fever in SLE:

Risk Factors for Infection:3

Laboratory Studies:3

References:

Differential Diagnosis and Evaluation of Hyponatremia

Differential Diagnosis and Evaluation of Hypernatremia

Differential Diagnosis and Evaluation of Hypokalemia

Differential Diagnosis of Hyperkalemia

Differential Diagnosis of Hypo and Hypercalcemia

Differential Diagnosis of Hypo and Hypermagnesemia

Differential Diagnosis of Hypo and Hyperphosphatemia

References:

Ultrasound

CT Abdomen/Pelvis

Differential Diagnosis of Biliary Duct Dilation: 1,2,3

References:

Hospital Course:

Laboratory Studies

Imaging:

CT Abdomen/Pelvis with IV contrast

Assessment:

Definition of Acute Kidney Injury: 1

Staging of Acute Kidney Injury: 1

Management of Contrast-induced AKI: 2

Differential Diagnosis of Acute Kidney Injury: 3

Evaluation of AKI: 4

References:

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs/Studies:

Imaging:

Hepatorenal free fluid

Splenorenal Free Fluid

Pelvic Free Fluid

Pseudogestational Sac

Assessment/Plan:

Differential Diagnosis of First Trimester Abdominal Pain: 1

Initial Evaluation of First Trimester Abdominal Pain: 1

Features Associated with Ectopic Pregnancy: 1

Ultrasonographic Findings in the Evaluation of Ectopic Pregnancy: 2

Contraindications to Medical Management: 2,3

References:

Appendicitis

Common Bile Duct

Cellulitis

Fetal Heart Rate

Free Fluid

Hydronephrosis

Thoracic Aorta Aneurysm

Pericardial Effusion

Inferior Vena Cava

B-lines

"Shred" sign

Pneumothorax

HPI:

PMH:

PSH:

FH:

Differential Diagnosis of Hypocalcemia: ^1,2

Laboratory Evaluation of Hypocalcemia: ^1,2

Clinical Manifestations of Hypocalcemia: ¹

Management of Symptomatic Hypocalcemia: ¹

Risk Factors for Infection:³

Laboratory Studies:³

Differential Diagnosis of Biliary Duct Dilation: ^1,2,3

Definition of Acute Kidney Injury: ¹

Staging of Acute Kidney Injury: ¹

Management of Contrast-induced AKI: ²

Differential Diagnosis of Acute Kidney Injury: ³

Evaluation of AKI: ⁴

Differential Diagnosis of First Trimester Abdominal Pain: ¹

Initial Evaluation of First Trimester Abdominal Pain: ¹

Features Associated with Ectopic Pregnancy: ¹

Ultrasonographic Findings in the Evaluation of Ectopic Pregnancy: ²

Contraindications to Medical Management: ^2,3

Mechanisms of Lower Extremity Edema: ¹

Differential Diagnosis of Lower Extremity Edema: ^1,2

History ^1,2

Physical Exam ^1,2

Key Features Distinguishing Cellulitis: ³

Skin and soft-tissue layers and their infections: ¹

Necrotizing Soft-Tissue Infections (NSTI):^2,3,4

LRINEC score ⁵

Pathophysiology of Acute Respiratory Distress Syndrome (ARDS):¹

Definition of ARDS (Berlin):^2,3

Causes of ARDS:^2,4

An Introduction to Mechanical Ventilation:^5,6,7