Elevated Hemidiaphragm

Causes of an Elevated Hemidiaphragm

References:

Lavender, JP, Potts DG (1959). Differential diagnosis of elevated right diaphragmatic dome. The British journal of radiology, 32(373), 56–60.
Nason, L. K., Walker, C. M., McNeeley, M. F., Burivong, W., Fligner, C. L., & Godwin, J. D. (2012). Imaging of the diaphragm: anatomy and function. Radiographics : a review publication of the Radiological Society of North America, 32(2), E51–70. doi:10.1148/rg.322115127
Prokesch, R. W., Schima, W., & Herold, C. J. (1999). Transient elevation of the hemidiaphragm. The British journal of radiology, 72(859), 723–724.
Burgener, F., Kormano, M. & Pudas, T. (2008). Differential diagnosis in conventional radiology. Stuttgart New York: Thieme.

Renal Failure in Cirrhosis

CC:

Consult for acute kidney injury

HPI:

63M with a history of liver cirrhosis of cryptogenic etiology, portal vein thrombosis, and esophageal varices s/p banding (2011) who was admitted to an OSH for altered mental status and hypotension requiring dopamine and was transferred to this facility for a higher level of care.

The nephrology service was consulted for elevated serum creatinine concerning for AKI. The patient has a baseline creatinine of 1.1 (3/2013), 1.9 on transfer and continued worsening to peak of 2.6 today.

PMH:

Asthma
COPD
Cirrhosis (PVT, encephalopathy)
Inguinal hernia (recurrent)

PSH:

Appendectomy
Bilateral inguinal hernia repair

FH:

Non-contributory

SHx:

Married
Denies t/e/d use

Meds:

albumin 25g i.v. q.6.h.
erythromycin 1,000mg p.o. q.1.h.
fluticasone-salmeterol 1 puff b.i.d.
lactulose 45g p.o. q.6.h.
neomycin 1,000mg p.o. q.1.h.
pantoprazole 40mg i.v. daily
rifaximin 550mg p.o. b.i.d.
sodium benzoate 5g p.o. b.i.d.

Allergies:

Sulfa

Physical Exam:

VS:	T	37.4	HR	90	RR	15	BP	86/48	O2	97% RA
Gen:	Chronically ill-appearing.
HEENT:	PERRL, scleral icterus, MMM
CV:	RRR
Lungs:	CTAB
Abd:	+BS, soft, non-tender, non-distended
GU:	Large ascites filled scrotum, testicles/inguinal canal not easily palpated
Ext:	Warm, well-perfused
Skin:	No palmar erythema, no vascular spiders
Neuro:	AAOx4, CN II-XII grossly intact

Labs:

BMP: 134/4.5/103/20/41/3.0/106 (Ca 9.3, Mg 3.7, PO4 2.4)
LFT: AST 89, ALT 33, TB 26.6, CB 16.1, Alb 2.7
NH4 167

Imaging:

Pleural Effusion

Large right pleural effusion with underlying compressive atelectasis.

Cirrhosis and Portal Hypertension

Shrunken/nodular liver with sequelae of portal hypertension including perisplenic collaterals, and splenomegaly.

SMV Thrombosis

Near-total thrombosis of the portal vein extending down to superior mesenteric vein.

B/L Inguinal Hernias

Large volume abdominal ascites with a large amount of fluid extending into the bilateral inguinal canals.

Large Right Inguinal Hernia

Large volume abdominal ascites with a large amount of fluid extending into the bilateral inguinal canals.

CT Abdomen/Pelvis (PVT)

Assessment/Plan:

63M with a history of liver cirrhosis of cryptogenic etiology, recently with hypotension prior to transfer to this facility and increase in creatinine from 1.9-3.0 on current admission (from baseline 1.1).

These findings indicate acute kidney injury, likely hepatorenal syndrome vs. acute tubular necrosis 2/2 prolonged hypotension. Plan to discontinue diuretics and start albumin challenge (1g/kg/day divided q6h x2d). Will also check UA, urine Na/cr/urea/eos, renal US (evaluate obstruction, kidney size). Start midodrine/octreotide for underlying HRS.

Neuro: Intermittent confusion. Lactulose, rifaximin, benzoate.
Resp: 2L NC. ABG 7.36/51/87/27.7/+2. CXR: Large R effusion.
CV: Levo 0.075. Midodrine 15 TID. MAPs 60, HR 80s.
GI: NPO/NGT. TPN.
Renal: See above.
Heme: Coagulopathy, keep INR <2.5
ID: Afebrile. No abx.
Endo: Euglycemic

Renal Failure in Cirrhosis:

Renal failure in cirrhosis is associated with higher mortality both before and after transplant. The main causes of renal failure in cirrhosis are detailed below, with particular attention to an entity unique to cirrhosis: the hepatorenal syndrome.¹

Disorder	Pathogenesis	Diagnosis	Management
HRS	Dilation of splanchnic arteries initially compensated by increased CO eventually decompensates with activation of mechanisms to preserve ECBV (RAAS, SNS, ADH) leading to fluid retention (ascites, edema) and renal failure due to intrarenal vasoconstriction.Bacterial translocation and the resulting inflammatory response may contribute to splanchnic vasodilation (through production of vasoactive factors like NO).	Serum creatinine > 1.5mg/dl- Not reduced with 1g/kg albumin No confounding factors (2d off diuretics, no nephrotoxic agents, no shock, no e/o intrinsic renal disease) Type 1: doubling creatinine > 2.5mg/dL in <2wk Type 2: stable, slower progression	Vasoconstrictor therapy- Albumin Portasystemic shunting Renal replacement therapy Prevention Norfloxacin Albumin
Intrinsic renal	Some causes of liver disease are also associated with intrinsic renal pathology (ex. GN associated with HBV, HCV).	Proteinuria, hematuria Renal bx Active urinary sediment	Antiviral therapy if appropriate
Pre-renal AKI	Hemorrhage (GIB), fluid losses (excess diuresis, diarrhea from lactulose).	Suspected from patient history Low FENa, bland urine sediment	Hemorrhage: replace volume with fluids, blood products. Control bleeding. Discontinue diuretics, administer fluids if tolerated
ATN	Severe ischemic or toxic (NSAID’s, nephrotoxic medications)	Renal tubular epithelial cells favor ATN (granular casts common in ATN, HRS)	Withdraw therapy Avoid nephrotoxic agents

Pathophysiology of Hepatorenal Syndrome:

Evaluation:

The evaluation of suspected renal failure in patients with cirrhosis involves assessment of renal function for evidence of acute impairment, as well as analaysis of urine for protein or active sediment to suggest intrinsic renal disease (possibly warranting renal ultrasonography or biopsy). Additionally, patients should be evaluated for evidence of bacterial infection including assessment of ascites if present as SBP produces a more severe form of the inflammatory vasodilation mechanism suspected to play a role in HRS.

Treatment:

For renal failure not caused by the hepatorenal syndrome, identification and management of the underlying cause is critical (intrinsic renal disease, hypovolemia/hemorrhage, nephrotoxicity, infection). For suspected HRS, management is dependent on the acuity and setting. In the intensive care unit, vasoconstrictor therapy (norepinephrine, vasopressin) in association with albumin is effective in the treatment of HRS.^2,3 In less acute settings, a combination of midodrine, octreotide and albumin improves renal function and is associated with lower short-term mortality.⁴ Alternatives for patients who do not respond to medical therapy include TIPS, dialysis and transplant.

Summary:

Renal failure in ESLD is due to the causes, complications or management of cirrhosis and has important implications, with HRS in particular offering the worst prognosis.⁵ Early recognition and management is critical to improving outcomes.

References:

Ginès, P., & Schrier, R. W. (2009). Renal failure in cirrhosis. The New England journal of medicine, 361(13), 1279–1290. doi:10.1056/NEJMra0809139
Singh, V., Ghosh, S., Singh, B., Kumar, P., Sharma, N., Bhalla, A., Sharma, A. K., et al. (2012). Noradrenaline vs. terlipressin in the treatment of hepatorenal syndrome: a randomized study. Journal of hepatology, 56(6), 1293–1298. doi:10.1016/j.jhep.2012.01.012
Kiser, T. H., Fish, D. N., Obritsch, M. D., Jung, R., MacLaren, R., & Parikh, C. R. (2005). Vasopressin, not octreotide, may be beneficial in the treatment of hepatorenal syndrome: a retrospective study. Nephrology, dialysis, transplantation, 20(9), 1813–1820. doi:10.1093/ndt/gfh930
Esrailian, E., Pantangco, E. R., Kyulo, N. L., Hu, K.-Q., & Runyon, B. A. (2007). Octreotide/Midodrine therapy significantly improves renal function and 30-day survival in patients with type 1 hepatorenal syndrome. Digestive diseases and sciences, 52(3), 742–748. doi:10.1007/s10620-006-9312-0
Alessandria, C., Ozdogan, O., Guevara, M., Restuccia, T., Jiménez, W., Arroyo, V., Rodés, J., et al. (2005). MELD score and clinical type predict prognosis in hepatorenal syndrome: relevance to liver transplantation. Hepatology (Baltimore, Md.), 41(6), 1282–1289. doi:10.1002/hep.20687

Macroscopic Hematuria

CC:

Macroscopic hematuria

HPI:

85yo male with a history of prostate cancer s/p radiation and androgen deprivation therapy four years ago complicated by urethral strictures requiring chronic indwelling catheter who presented to the ED yesterday with 3 days of red urine followed by no output from catheter and abdominal pain. In the ED, the patient was found to have stable hemoglobin and creatinine and was discharged with urology follow-up after symptom resolution with catheter irrigation.

Today, the patient reports no new issues, denies abdominal/flank pain, further catheter obstruction, fevers/chills. He states that his urine has been light pink in color, without clots, and significantly more clear than the prior 3 days. He has had intermittent episodes of blood in his urine in the past, but never causing obstruction. His catheter is managed at home with regular (q3wk) changes and no recent traumatic catheterizations.

He denies any new back/bone pain or unintentional weight loss.

PMH:

Prostate CA
HTN
DM
CKD
CAD

PSH:

None

FH:

Non-contributory

SHx:

No current or previous t/e/d use
Lives with wife

Meds:

lisinopril 20mg p.o. daily
glyburide/metformin 1.25/250mg p.o. b.i.d.
atorvastatin 20mg p.o. daily
ASA 81mg p.o. daily

Allergies:

NKDA

Physical Exam:

VS:	T	98.4	HR	64	RR	13	BP	136/94	O2	99% RA
Gen:	Well-appearing, pleasant man in no acute distress.
Abd:	+BS, soft, NT/ND, no suprapubic tenderness, no CVAT
GU:	Foley catheter in place draining clear-pink fluid to leg bag, no clots. No evidence of trauma to urethra, no visible skin lesions. Testes descended bilaterally, no inguinal lymphadenopathy.

Assessment/Plan:

85M hx CaP (2009) s/p radiation and androgen deprivation therapy with urethral strictures requiring chronic indwelling catheter presenting with macroscopic hematuria. Given patient’s history, radiation cystitis is a likely cause of his symptoms. However, given the long-standing catheter, other considerations include trauma and infection. Also, recurrence or new malignancy must be considered. Will obtain UA, UCx, and schedule patient for cystoscopy with bilateral retrograde pyelogram. Also, educated patient on how to irrigate catheter if needed and provided ED precautions should obstruction persist despite irrigation attempts. Patient’s last surveillance PSA undetectable, continue routine follow-up.

Differential Diagnosis of Macroscopic Hematuria

Important Historical Elements:

Painless: suggests malignancy
Painful: suggests calculi/infection
Urinalysis: presence of dysmorphic RBC’s, RBC/WBC casts, proteinuria suggest intrinsic renal disease
Timing: early (distal urethra), throughout (upper urinary tract), terminal (bladder neck, prostatic)

Guided Lecture

Watch “Gross Hematuria: Just a Bit of Kool-Aid” from EM Ed. In this lecture Dr. Basrai reviews the differential diagnosis and management of macroscopic hematuria in the emergency department.

References:

Hicks, D., & Li, C.-Y. (2007). Management of macroscopic haematuria in the emergency department. Emergency medicine journal : EMJ, 24(6), 385–390. doi:10.1136/emj.2006.042457
Mazhari, R., & Kimmel, P. L. (2002). Hematuria: an algorithmic approach to finding the cause. Cleveland Clinic journal of medicine, 69(11), 870–872–4– 876.
Howes DS, Bogner MP. Chapter 94. Urinary Tract Infections and Hematuria. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds.Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. http://www.accessmedicine.com/content.aspx?aID=6362340. Accessed June 14, 2013.
Sutton, J. M. (1990). Evaluation of hematuria in adults. JAMA : the journal of the American Medical Association, 263(18), 2475–2480.

Hyperbilirubinemia

CC:

Yellow eyes

HPI:

51yo AA male with hx DM, HTN, sarcoidosis presents with yellowing of eyes and full-body itching x3wks. This was associated with dark urine and loose, light-brown stools. He denies N/V, abdominal pain, PO intolerance, F/C, recent travel, weight loss. He states that this has not occurred in the past, and he does not have any prior history of post-prandial abdominal pain.

PMH:

DM
HTN
Sarcoidosis

PSH:

None

FH:

No GI malignancy

SHx:

No tobacco or drug use, 10 years of 10 drinks/wk stopped 1yr ago

Meds:

lisinopril 20mg p.o. daily
pioglitazone 15mg p.o. daily
sitagliptin 100mg p.o. daily
lansoprazole 15mg p.o. daily

Allergies:

Vicodin (rash)

Physical Exam:

VS:	T	97.9	HR	102	RR	12	BP	128/68	O2	99% RA
Gen:	WA, NAD
HEENT:	Marked scleral icterus, PERRL, yellowing of posterior oropharynx and floor of mouth, MMM, no cervical lymphadenopathy
CV:	RRR, S1/S2 normal, no murmurs
Lungs:	CTAB with good air movement
Abd:	Obese, +BS, soft, NT/ND, no rebound/guarding, no palpable organomegaly, negative Murphy
GU:	No inguinal lymphadenopathy
Ext:	Warm, well-perfused, no LE edema, peripheral pulses 2+
Skin:	No visible skin lesions
Neuro:	AAOx3

Labs:

CBC: 16/12.4/35.1/281
LFT: AST 281, ALT 302, AP 264, T.bili 22.1, D.bili 16.8

Studies:

RUQ US: Biliary sludge, no stones, no GBW thickening, no pericholycystic fluid
ERCP: 3cm stricture of distal CBD, biopsies taken

Assessment/Plan:

51AAM w/DM, HTN, sarcoidosis with 3wks painless jaundice. Obstructive pattern along with only modest elevation of liver enzymes suggests the obstruction is likely extrahepatic which was supported by ERCP finding of a distal CBD stricture. Patient has no history of prior instrumentation to cause iatrogenic stricture, and while sarcoidosis is associated with cholestatic complications (portal granulomas), pathology from biopsy showed papillary adenocarcinoma. The patient was scheduled for surgery with a plan for initial laparoscopic survey of the abdomen followed by Whipple if no evidence of widespread disease.

Imaging:

ERCP

3cm stricture of distal CBD

MRCP

Filling defect in the common bile duct with marked dilatation of the common duct and intrahepatic ducts.
Findings may reflect an intraluminal mass or stone.

CT Abdomen/Pelvis

Common bile duct stent present
Expected air in the intrahepatic biliary tree and mild biliary ductal dilatation

Differential Diagnosis of Hyperbilirubinemia: ^{1, 2}

Evaluation of Hyperbilirubinemia: ³

References:

Heathcote, E. J. (2007). Diagnosis and Management of Cholestatic Liver Disease. Clinical Gastroenterology and Hepatology, 5(7), 776–782. doi:10.1016/j.cgh.2007.05.008
Hirschfield, G. M., Heathcote, E. J., & Gershwin, M. E. (2010). Pathogenesis of cholestatic liver disease and therapeutic approaches. Gastroenterology, 139(5), 1481–1496. doi:10.1053/j.gastro.2010.09.004
McGill, J. M., & Kwiatkowski, A. P. (1998). Cholestatic liver diseases in adults. The American Journal of Gastroenterology, 93(5), 684–691. doi:10.1111/j.1572-0241.1998.206_a.x

Nausea and Vomiting

HPI:

57yo male with a history of HTN, DM, and MI s/p stent in 2011 presenting with nausea/vomiting and hypotension. The patient had one episode of non-bloody, non-bilious emesis approximately 6 hours ago. He felt unwell so a friend checked his blood pressure which was found to be 75/50, prompting a visit to this emergency department.
The patient’s emesis came 2 hours following a normal meal (frozen dinner), and was associated with chills/sweats but no abdominal pain. The patient had some associated shortness of breath (baselines), but no chest pain, arm or jaw pain, or palpitations.

He states that these symptoms are unlike what he experienced during his MI. He reported no change in bowel or urinary habits.

PMH:

HTN
DM
CAD
MI
Hyperlipidemia

PSH:

Stent placement (2011)
Right knee neuroma excision (2012)

FH:

Non-contributory

SHx:

No current t/e/d
80 pack-year smoking history

Meds:

carvedilol 6.25mg p.o. b.i.d.
metformin 1000mg p.o. b.i.d.
atorvastatin 20mg p.o. daily
aspirin 81mg p.o. daily

Allergies:

NKDA

Physical Exam:

VS:	T	98.4	HR	65	RR	17	BP	96/56	O2	95% 2L NC
Gen:	No acute distress, speaking in complete sentences
HEENT:	PERRL, MMM no lesions, no cervical lymphadenopathy
CV:	RRR, normal S1/S2, no murmurs, no extra heart sounds, no jugular venous distension
Lungs:	CTAB, no crackles
Abd:	+BS, soft, NT/ND, no rebound/guarding, no organomegaly
Ext:	Warm, well-perfused, peripheral pulses equal b/l, no LE edema
Neuro:	AAOx3

Labs:

EKG: normal sinus rhythm, anterior lead q-waves suggestive of old infarct, no T/ST changes
Troponin: <0.01
CBC: 7.4/15.5/47/228
BMP: 139/5.1/107/26/8/1.19/112 (baseline creatinine 1.06 in 2/2013)

Studies:

CXR: no effusion, no cardiomegaly, no focal consolidation
Bedside US: normal cardiac wall motion, estimated EF 40-45%, retrohepatic IVC collapses with respiration

Assessment/Plan:

57M hx HTN, DM, MI s/p stent presenting with nausea/vomiting x1 and hypotension. The patient’s symptoms and history were concerning for acute myocardial infarction; however, early EKG and troponins were reassuring. Additionally, the absence of characteristic physical findings that would be associated with an acute MI causing cardiogenic shock (elevated JVP, extra heart sounds, pulmonary crackles) were not present. Evidence of end-organ damage was also absent.

Other potential causes for nausea/vomiting include SBO, however, the patient reported normal BM’s and has no history of abdominal surgery. Though occurring after a meal, a single episode of emesis without associated abdominal pain lowers suspicion for biliary disease. This patient’s emesis is most likely due to acute gastroenteritis.

Given the evidence of hypovolemia on bedside ultrasound, the patient was bolused with a total of 1.5L NS and noted symptomatic improvement as well recovery of blood pressure.

Differential Diagnosis of Nausea/Vomiting: ^{1, 2}

Pathophysiology: ^{3, 4, 5}

Nausea: Sensation associated with increased gastrointestinal motility (tachygastria).
Vomiting:
- Chemoreceptor trigger zone (area postrema of 4^th ventricle): sensitive to drugs/toxins (emetics, radiation), neurotransmitters. Located outside BBB.
- Nucleus tractus solitaries (medulla): pattern generator for vomiting, receives vagal input from GI tract and nociceptive stimuli from peripheral nervous system – transmits to hypothalamus, limbic system and cortex. Stimulated by tickling the back of the throat, gastric distention, and vestibular input.

Important history/physical associations: ⁴

Abdominal pain: suggests organic disease, affected organ dependent on location of pain. (See figure)
Abdominal distension: suggests bowel obstruction.
Heartburn: suggests GERD.
Vertigo/nystagmus: suggests vestibular etiology.
Positional/projectile: suggests neurogenic etiology.

Differential Diagnosis of Abdominal Pain By Location:

References:

Scorza, K., Williams, A., Phillips, J. D., & Shaw, J. (2007). Evaluation of nausea and vomiting. American family physician, 76(1), 76–84.
Bork S, Ditkoff J, Hang BS. Chapter 75. Nausea and Vomiting. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. http://www.accessmedicine.com/content.aspx?aID=6360091. Accessed June 15, 2013.
Koch, K. L., Stern, R. M., Vasey, M. W., Seaton, J. F., Demers, L. M., & Harrison, T. S. (1990). Neuroendocrine and gastric myoelectrical responses to illusory self-motion in humans. The American journal of physiology, 258(2 Pt 1), E304–10.
Longstreth, G. F. Approach to the adult with nausea and vomiting. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
Costanzo, L. (2011). Physiology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Patanwala, A. E., Amini, R., Hays, D. P., & Rosen, P. (2010). Antiemetic therapy for nausea and vomiting in the emergency department. The Journal of emergency medicine, 39(3), 330–336. doi:10.1016/j.jemermed.2009.08.060

Hemoptysis

Source: Mulpuru, S., Touchie, C., Karpinski, J., & Humphrey-Murto, S. (2010). Coexistent Wegener“s granulomatosis and Goodpasture”s disease. The Journal of rheumatology, 37(8), 1786–1787. doi:10.3899/jrheum.091404

Linear IgG deposits consistent with anti-GBM disease.

CC:

“bad cough”

HPI:

61yo African American female w/hx of HTN presenting with 1mo of persistent cough productive of green-yellow sputum, noticed streaks of blood for the past 5 days. She came to the ED today because she has been feeling increasingly fatigued. She reports subjective fevers at the onset of symptoms which has resolved. She denies shortness of breath, chest pain, chills, night sweats. She sought medical care for this problem 2wk ago and was treated with amoxicillin and a cough suppressant. She recalls a coworker was ill one month ago. She is US-born, had a negative PPD in the past and has no known exposures to tuberculosis.

Of note, the patient reports her urine had a foamy appearance and has been darker in color beginning 3 weeks ago, but this had resolved. She denied dysuria, or frank hematuria.

PMH:

HTN
Asthma – last required medications >30yrs ago

PSH:

None

FH:

Non-contributory

SHx:

No t/e/d
Works as librarian

Meds:

benazepril
amlodipine
amoxicillin
promethazine

Allergies:

NKDA

Physical Exam:

VS:	T	99.4	HR	97	BP	132/60	RR	20	O2	92%
Gen:	Well-appearing, pleasant, speaking in complete sentences
HEENT:	PERRL, MMM no lesions, no cervical lymphadenopathy
CV:	RRR, normal S1/S2, no murmur appreciated
Lungs:	Crackles in posterior: right middle/inferior and left inferior fields, no wheezing, no dullness to percussion
Abd:	+BS, soft, non-tender, no CVAT
Ext:	Warm, well-perfused, 2+ peripheral pulses, 1+ pitting edema to knee
Skin:	No lesions on exposed skin
Neuro:	AAO

Labs:

CBC: 12.3/6.7/19.8/52.3 (S: 94, B: 1, L: 4, M: 1, MCV: 92.3); baseline Hb/Hct (1/11/2012) 13.4
BMP: 136/3.6/101/25/46/3.43/126; baseline creatinine (1/11/2012) 1.18
UA: brown, trace LE, – nitrites, 2+ protein, 81 RBC

Imaging:

Right mid-lung zone consolidation is present, suggests pneumonia if acute.
Mild asymmetric right parenchymal increased density is seen diffusely as well.

Assessment/Plan:

65AAF w/hx HTN presents with persistent productive cough, recently with hemoptysis.

# Cough: Symptoms and physical findings of abnormal breath sounds (crackles, though no strict consolidation) concerning for community-acquired pneumonia. Addition of hemoptysis raises concern for TB, particularly when taking into consideration the duration of cough and presence of constitutional symptoms. CBC shows leukocytosis with left shift, CXR with right mid/lower lob infiltrates consistent with pneumonia. Recommend admission and isolation to rule out TB, start empiric therapy for community acquired pneumonia with ceftriaxone, azithromycin. Obtain induced sputum samples for culture, AFB smear and culture.

# Abnormal urine: Patient describes changes in urine suggestive of proteinuria and hematuria. Acuity of onset and apparent spontaneous resolution suggests a chronic kidney injury 2/2 hypertension is unlikely. Absence of dysuria, or tenderness (suprapubic, costovertebral) suggests complicated UTI unlikely. Urinalysis notable for 2+ protein and significant RBC’s, possible nephritic syndrome. In the setting of hemoptysis, this raises concern for anti-GBM disease vs. vasculitis.

# Anemia: Normocytic anemia. No evidence of acute, life-threatening hemorrhage as patient is currently hemodynamically stable. Possible sites of blood loss include alveoli, glomeruli. Given that patient sought care today for worsening fatigue, will monitor hemoglobin closely and consider transfusion. Obtain iron studies.

# HTN: BP stable, hold home medications.

Interval History:

The patient was admitted for management of community-acquired pneumonia and isolation to rule out TB. Empiric therapy with CTX + azithromycin was continued. On HOD1, the patient was transfused two units of PRBC’s. On HOD2, the patient underwent CT chest/abdomen/pelvis due to worsening respiratory status despite antimicrobial therapy. On HOD3, the patient went into atrial fibrillation with RVR which was converted to sinus rhythm with metoprolol 5mg IV x3. On HOD5, nephrology consult recommended starting steroid therapy, plasmapheresis and obtaining a renal biopsy, however the biopsy was delayed due to worsening respiratory status.

Interval Labs:

Iron studies: Fe 8, TIBC 203, Ferritin 468, haptoglobin 333, retics 2.7
Inflammatory markers: ESR 120, CRP 34
Micro: BCx NGTD, RCx moderate Candida, sputum AFB smear negative x3
LFT: AST 34, ALT 29, ALP 52, protein 6.3, albumin 2.4, T.bil 0.8, D.bil 0.2
Quant-gold: negative
Anti-GBM 1.2 (nl <1.0)
p-ANCA: positive 1:640, [ELISA pending]
ANA: positive 1:320, speckled
HIV: negative

Interval Imaging:

CT Chest

Diffuse right lung, tree and bud opacities, ground-glass opacities and areas of confluence with scattered air bronchograms. Less severe similar pattern in the left lung as well particular at the base.
Right paratracheal, subcarinal and perihilar LAD.
Findings concerning for primary TB in the right clinical setting. DDx nonspecific bacterial PNA and fungal PNA.

CT Abdomen/Pelvis

Mild nonspecific R > L perinephric stranding.

Interval Assessment/Plan:

# Acute respiratory failure: Unlikely simple CA-PNA given worsening status while on appropriate antibiotic therapy. Active tuberculosis possible given history of chronic productive cough with hemoptysis, constitutional symptoms and imaging findings. IGRA’s of limited utility in diagnosis of active disease, further, while three negative sputum AFB smears decreases the likelihood of TB, additional testing with NAAT and culture is required. Another possibility is a vasculitic process given concomitant hematuria and acute renal failure, with respiratory symptoms now 2/2 alveolar hemorrhage. This was evaluated with ANCA assay which was positive for p-ANCA with high titer. This is often suggestive of primary vasculitis (in this case likely microscopic polyangiitis vs. Churg-Strauss), however ELISA for target antigen is of particular importance as p-ANCA with specificity for antigens other than MPO can be associated with another condition on the differential: Goodpasture’s syndrome. This patient was found to have elevated anti-GBM antibodies which are highly suggestive of Goodpasture’s syndrome, and can be associated with ANCA-positivity (often suggesting a poorer prognosis with decreased likelihood of recovery of renal function).¹

# Acute kidney injury: The patient had significant elevation of serum creatinine compared to last-recorded baseline. She also described darkening and foamy appearance of urine 3 weeks prior to admission, suggestive of proteinuria/hematuria of relatively acute onset. This was supported by urinalysis findings of protein and RBC’s (with casts). Given presence of anti-GBM antibodies, high specificity of such findings, and correlation with glomerulonephritis with evidence of pulmonary alveolar hemorrhage, this appears to be the most likely cause at this time. Definitive diagnosis with renal biopsy to be obtained following stabilization of respiratory status. Patient will be started on plasmapheresis and immunosuppressive therapy (corticosteroids, cyclophosphamide).

# Normocytic Anemia: Likely combination of acute blood loss (2/2 hematuria, pulmonary alveolar hemorrhage) and chronic disease. Normocytic anemia with some reticulocytosis suggestive of acute blood loss, however iron studies with low Fe, TIBC and elevated ferritin suggest chronic disease as an associated factor.

Differential Diagnosis of Hemoptysis: ^{2, 3}

A System for the Diagnosis of Tuberculosis: ^{4, 5}

A System for Vasculitides: ^{8, 9}

Vasculitis Mimics: ⁹

Interpretation of antineutrophil cytoplasmic autoantibodies (ANCA): ¹⁰

Pattern	Target	Associated vasculitis	Other diseases
C-ANCA	PR3	Granulomatosis with polangiitis (Wegener’s) Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) Microscopic polyangiitis Pauci-immune glomerulonephritis
C-ANCA (atypical)	BPIMPO		IBD Cystic fibrosis
P-ANCA	MPO	Microscopic polyangiitis Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) Pauci-immune glomerulonephritis
P-ANCA	Non-MPO		Autoimmune hepatitis IBD, PSC SLE, RA Drugs Infection (HIV, fungal)

Differential Diagnosis of Anemias: ¹¹

References:

Levy, J. B., Hammad, T., Coulthart, A., Dougan, T., & Pusey, C. D. (2004). Clinical features and outcome of patients with both ANCA and anti-GBM antibodies. Kidney international, 66(4), 1535–1540. doi:10.1111/j.1523-1755.2004.00917.x
Bidwell, J. L., & Pachner, R. W. (2005). Hemoptysis: diagnosis and management. American family physician, 72(7), 1253–1260.
Hirshberg, B., Biran, I., Glazer, M., & Kramer, M. R. (1997). Hemoptysis: etiology, evaluation, and outcome in a tertiary referral hospital. Chest, 112(2), 440–444. doi:10.1378/chest.112.2.440
Campbell, I. A., & Bah-Sow, O. (2006). Pulmonary tuberculosis: diagnosis and treatment. BMJ (Clinical research ed.), 332(7551), 1194–1197. doi:10.1136/bmj.332.7551.1194
Zumla, A., Raviglione, M., Hafner, R., & Reyn, von, C. F. (2013). Tuberculosis. The New England journal of medicine, 368(8), 745–755. doi:10.1056/NEJMra1200894
Diagnostic Standards and Classification of Tuberculosis in Adults and Children. American journal of respiratory and critical care medicine. doi:10.1164/ajrccm.161.4.16141
Laraque, F., Griggs, A., Slopen, M., & Munsiff, S. S. (2009). Performance of nucleic acid amplification tests for diagnosis of tuberculosis in a large urban setting. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 49(1), 46–54. doi:10.1086/599037
Gross, W. L., Trabandt, A., & Reinhold-Keller, E. (2000). Diagnosis and evaluation of vasculitis. Rheumatology (Oxford, England), 39(3), 245–252.
Suresh, E. (2006). Diagnostic approach to patients with suspected vasculitis. Postgraduate medical journal, 82(970), 483–488. doi:10.1136/pgmj.2005.042648
Rus, V., & Handwerger, B. S. (2000). Clinical value of antineutrophil cytoplasmic antibodies. Current rheumatology reports, 2(5), 383–389.
Goljan, E. (2011). Pathology. Philadelphia, PA: Mosby/Elsevier.

Small Bowel Obstruction

CC:

Consultation for bowel obstruction

HPI:

The patient is a 40yo male with a history of alcohol abuse, and seizure disorder secondary to traumatic brain injury who was admitted to this hospital 4d ago after an altercation with law enforcement officials. On arrival, the patient was reported to be acutely intoxicated with ecchymosis and bleeding from left lateral/posterior head and ear. No other significant injuries were found and the patient underwent CT imaging of head and c-spine, with notable findings of left occipital epidural hematoma, subarachnoid hemorrhage, but no significant midline shift. Neurosurgery was consulted and no emergent surgical intervention was required, the patient underwent serial imaging to monitor the bleed which was found to be stable and the patient slowly returned to baseline mental status.

On HOD4, the patient developed nausea/vomiting and abdominal pain, a nasogastric tube was placed with feculent output. CT abdomen/pelvis showed high grade SBO and possible mesenteric ischemia/infarct, and general surgery was consulted for further evaluation. The patient reported experiencing some abdominal pain since the altercation, but could not recall if he was hit in the abdomen.

PMH:

Alcohol abuse
Seizure disorder

PSH:

Tibia fracture
No prior abdominal surgery

FH:

Non-contributory

SHx:

Current alcohol, marijuana use, no tobacco use
History of homelessness

Medications:

Norco PRN
Ativan PRN
LISS, SQH, Thiamine
NKDA

Physical Exam:

VS: T 99.5°F HR 108 RR 16 BP 128/82 O2 99% RA
Gen: NAD
HEENT: PERRL, EOMI, sclera clear, anicteric
CV: RRR, normal S1/S2
Lungs: CTAB
Abd: Distended, diffuse tenderness to palpation, no rebound tenderness, no ecchymoses or signs of trauma
Ext: Warm, well-perfused
Neuro: AAOx4, appropriate

Assessment/Plan:

40M w/hx alcohol abuse, TBI and seizure disorder, presented initially with evidence of head trauma which was stabilized. However, the development of abdominal pain, N/V, and finding of distension on exam associated with copious output of feculent material from NGT suggests bowel obstruction. This patient has no history of abdominal surgeries to suggest adhesions as a possible cause. Though the patient cannot recall any abdominal trauma, and there was no e/o trauma on exam, findings on CT abdomen/pelvis are suggestive of traumatic cause (hematoma causing obstruction or ischemia resulting from mesenteric injury). The patient was monitored for several days, continuing NGT to suction and with serial abdominal films. However, abdominal pain persisted, abdominal radiographs showed worsening obstruction and the patient developed leukocytosis and on HOD7 the patient was taken to the OR for exploratory laparotomy. Upon entering the peritoneal cavity, there was obvious blood and very distended small bowel which was run distally with finding of a mesenteric laceration in the distal ileum which was walled off by omentum. Additionally, a grade 2 splenic laceration was found. Ultimately, a small bowel resection with primary anastomosis along with a repair of the splenic laceration was performed.

Imaging:

CT abdomen/pelvis

Moderate abdominal and pelvic ascites which has Hounsfield unit attenuation is greater than simple fluid suggestive of blood products.

CT abdomen/pelvis

Fluid dilated small bowel

CT abdomen/pelvis

Complex transition point in the central mid abdomen.
Segment of bowel at the transition point has circumferential mural thickening and surrounding complex attenuation mesenteric fluid and mesenteric stranding.

Abdominal X-Ray

Small bowel distention
Nasogastric tube is seen coiled in the gastric fundus

CT Head

Left occipital extracranial soft tissue hematoma
Left occipital epidural hematoma subjacent to the fracture site in addition to subarachnoid hemorrhage within the sulci of the left temporal lobe and interpeduncular cistern
Extra-axial fluid collection along the right frontal convexity, tracking down the anterior falx, compatible with a subdural hematoma

Differential Diagnosis for bowel obstruction: ^{1, 2, 3}

Types of Abdominal Pain: ⁴

References:

Kulaylat MN, Doerr RJ. Small bowel obstruction. In: Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001. Available from: http://www.ncbi.nlm.nih.gov/books/NBK6873/
Jackson, P. G., & Raiji, M. T. (2011). Evaluation and management of intestinal obstruction. American family physician, 83(2), 159–165.
Maung, A. A., Johnson, D. C., Piper, G. L., Barbosa, R. R., Rowell, S. E., Bokhari, F., Collins, J. N., et al. (2012). Evaluation and management of small-bowel obstruction. Journal of Trauma and Acute Care Surgery, 73, S362–S369. doi:10.1097/TA.0b013e31827019de
Stabile, Bruce. “The Acute Abdomen.” Chairman’s Hour. Harbor UCLA Department of Surgery Student Lecture Series. 5/17/13. Lecture.

Abdominal Wall Hernias

HPI:

23M w/no known medical history presenting with abdominal “ball” x10d. Patient denies pain, and is tolerating regular diet w/o N/V. Reports lifting weights.

PMH/PSH/FHx/SHx:

None, non-contributory, no t/e/d.

Meds:

Acetaminophen, NKDA

PE:

VS: T N/A HR 86 RR 18 BP 116/64 O2 N/A
Gen: Well-appearing young male, no acute distress
HEENT: PERRL, MMM no lesions
CV: RRR, normal S1/S2, no murmurs
Lungs: CTAB, no crackles/wheezes
Abd: +BS, soft, NT/ND, 3cm bulge in right inguinal region with valsalva, above inguinal ligament, ~7cm lateral to symphysis, non-tender, reduces spontaneously after valsalva GU: uncircumcised penis, testes descended b/l, normal size, non-tender, no herniation through inguinal canal palpated with valsalva
Ext: Warm, well-perfused, 2+ peripheral pulses
Neuro: Alert and oriented, appropriate

Assessment/Plan:

23M ċ inguinal hernia, currently asymptomatic with no evidence of incarceration/strangulation. Recommend follow-up at city hospital for evaluation and possible surgical repair. Advised to refrain from strenuous activity, heavy lifting.

Physical Examination Techniques: ¹

Observation: Best performed with patient standing and physician seated on a stool facing the patient
Palpation: place hand over patient’s groin (see figure), with two fingers each superior and inferior to the inguinal ligament. Have the patient cough and feel for a palpable bulge or impulse.
GU: With a finger in the inguinal canal, bulges felt against the side of the examining finger are direct hernias, while those felt at the tip of the finger are indirect.

Types of Abdominal Wall Hernias: ²

Name	Location	Etiology/Epidemiology
1. Umbilical	Linea alba through weakened umbilical ring.Paraumbilical hernias through linea alba in the region of the umbilicus.	Congenital or acquired due to increased intra-abdominal pressure (obesity, pregnancy, ascites, PD)
2. Epigastric	Linea alba between umbilicus and xiphoid process	Congenital weakness of linea alba (lack of decussating fibers)
3. Spigelian	Semilunar line: along the lateral borders of rectus abdominus. Herniation typically occurs caudally (below arcuate line) due to absence of posterior rectus sheath.
4. Incisional	Site of prior incision	Poor fascial healing possibly due to: infection (increased risk in wound dehiscence), obesity, smoking, immunosuppression excess wound tension, CT disorders.
5. Inguinal	Indirect: internal (deep) inguinal ring, lateral to inferior epigastric vessels.Direct: external (superficial) inguinal ring, medial to inferior epigastric vessels.	Indirect > direct.
6. Femoral	Inferior to the inguinal ligament, through empty space medial to femoral sheath.	F > M, increased likelihood of incarceration/strangulation (40%)
7. Lumbar ³	Arise in two anatomical triangles:Superior lumbar triangle – lateral border internal oblique, medial border erector spinae, superior border 12^thrib.Inferior lumbar triangle – lateral border external oblique, medial border latissimus dorsi, inferior border iliac crest. (See figure)	Associated with surgery (incisional), typically urologic.
8. Obturator	Protrusion of peritoneal sac through obturator foramen.	Rare, occur primarily in elderly women (high predisposition for incarceration).

Locations of Abdominal Wall Hernias:

Layers of the Anterior Abdominal Wall:

Differential diagnosis for groin masses: ⁴

Category	Inguinal ⁵	Scrotal ⁶	Vulvar ⁷	Perineal ⁸
Vascular	Varicocele extension	Varicocele	Vulvar varicocity Hemangioma
Infectious, Inflammatory	Lymphadenopathy Abscess Inflammatory joint process (hip, related bursae) Thrombophlebitis	Epididymitis Epididymo-orchitis	Condyloma Molluscum Bartholin’s cyst
Neoplastic	Benign (lipoma) Lymph node metastatsis	Testicular malignancy	Malignant skin lesions	Soft-tissue malignancy Anal SCC Rectal GIST Metastasis (commonly anorectal, prostatic)
Congenital, Anatomic	Hernia Testis (undescended, retracted)	Epididymal cyst Spermatocele Hydrocele	Embryological remnants (mucocele)
Traumatic	Hematoma Aneurysm (complication of catheterization)	Hematoma	Hematoma

Locations of Groin Masses: ⁹

References:

Amerson JR. Inguinal Canal and Hernia Examination. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 96. Available from: http://www.ncbi.nlm.nih.gov/books/NBK423/
Aguirre, D. A., Casola, G., & Sirlin, C. (2004). Abdominal Wall Hernias: MDCT Findings. American Journal of Roentgenology, 183(3), 681–690. doi:10.2214/ajr.183.3.1830681
Guillem, P., Czarnecki, E., Duval, G., Bounoua, F., & Fontaine, C. (2002). Lumbar hernia: anatomical route assessed by computed tomography. Surgical and radiologic anatomy : SRA, 24(1), 53–56.
Roberts, J. R., & Hedges, J. R. (2010). Clinical procedures in emergency medicine. (5th ed., Vol. section 7, p. Ch. 44). W B Saunders Co. Retrieved from http://www.mdconsult.com/books/page.do?eid=4-u1.0-B978-1-4160-3623-4.00044-4
Shadbolt, C. L., Heinze, S. B., & Dietrich, R. B. (2001). Imaging of groin masses: inguinal anatomy and pathologic conditions revisited. Radiographics : a review publication of the Radiological Society of North America, Inc, 21 Spec No, S261–71.
Eyre, RC. Evaluation of nonacute scrotal pathology in adult men. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2013.
Foster, D. C. (2002). Vulvar disease. Obstetrics and gynecology, 100(1), 145–163.
Tappouni, R. F., Sarwani, N. I., Tice, J. G., & Chamarthi, S. (2011). Imaging of unusual perineal masses. American Journal of Roentgenology, 196(4), W412–20. doi:10.2214/AJR.10.4728
Collins, R. (2008). Differential diagnosis in primary care. Philadelphia: Lippincott Williams & Wilkins.

Case Photos from Jalapa

$Greenstick fracture$

$Posterior rib fracture with hematoma$

Acute Diarrhea (in developing countries)

HPI:

1yo M, ex-term, previously healthy, with 8d tactile fever/diarrhea, initially watery, presenting now due to bloody diarrhea x1d. Mother reports 8-10 episodes/day, decreased PO intake and urine output x4d and changes in behavior (lethargy, irritability). No vomiting, no e/o abdominal pain, no cough, no seizures, no weight loss, no known sick contacts.

PMH:

Full term
No perinatal complications
Vaccination history unknown

SHx:

Meeting all developmental milestones
No sick contacts

PSH/FH/Meds/Allergies:

None

Physical Exam:

VS: HR 135 BP 86/60 RR 24 T N/A Wt 11kg (60%)
General: Patient was initially examined after initial rehydration with IVF. Well-appearing child, interactive and smiling.
HEENT: NC/AT, PERRL, MMM no lesions, no nuchal rigidity
CV: RRR, normal S1/S2
Lungs: CTAB
Abd: +BS, soft, NT/ND, no rebound/guarding
Ext: Warm, well-perfused, 2+ peripheral pulses (radial, DP, PT), capillary refill <2s
Skin: No visible skin lesions
Neuro: Alert and responsive

Assessment/Plan:

1yo healthy male with fever, bloody diarrhea and history consistent with dehydration. Most likely cause of acute diarrhea in this patient is infectious, particularly Shigella spp given presence of blood. Other concerning causes of diarrhea in this patient with reports of fever and changes in mental status include a serious bacterial illness (meningitis, pneumonia, UTI), however, these are less likely given the predominant, voluminous diarrhea and absence of symptoms associated with each. Other considerations include appendicitis, volvulus, intussusception, however again copious diarrhea in association with a benign abdominal exam makes these causes less likely. Early presentation of chronic diarrhea cannot be ruled out, however unlikely given association with fever and local prevalence of infectious causes.

Management included IV rehydration, followed by maintenance with PO ORS, early nutritional support, and ciprofloxacin 15mg/kg IV q12h.

Types and causes of acute diarrhea: ^{1, 2}

Assessment of Hydration Status

	Dehydration Level
Variable/Sign	Mild (3-5%)	Moderate (6-9%)	Severe (>10%)
General appearance	Restless, alert	Drowsy, postural hypotension	Limp, cold, sweaty, cyanotic extremities
Radial pulse	Normal rate, strength	Rapid, weak	Rapid, thready, sometimes impalpable
Respiration*	Normal	Deep	Deep and rapid
Anterior fontanelle	Normal	Sunken	Very sunken
SBP	Normal	Normal or low	Low
Capillary refill*	Normal (<2s)	Prolonged (2-4s)	Markedly prolonged (>4s)
Skin turgor*	Normal	Pinch retracts slowly	Pinch retracts very slowly
Eyes	Normal	Sunken	Grossly sunken
Tears	Present	Absent	Absent
Mucous membranes	Moist	Dry	Very Dry

* = sensitivity > 70% ^3,4

Management of Acute Diarrhea: ^5,6

Pathogens causing diarrhea: ⁶

Pathogen	Epidemiology/Transmission	Comments	Incubation	Fever	Abd. pain	N/V	Bloody stool	Stool WBC	Stool Heme
S. aureus, B. cereus	Food poisoning with preformed toxin	Vomiting > diarrhea	1-6h	X	–	✓	X	X	X
C. perfringens	Spores germinate in meats, poultry		6-24h	X	–	✓	X	X	X
Norovirus	Winter outbreaks in schools, nursing homes, cruise ships	Adults: diarrhea Children: vomiting	1-2d	–	✓	–	X	X	X
Rotavirus	#1 MCC children	Vaccine available	1-2d	–	✓	–	X	X	X
Campylobacter	#1 MCC invasive enterocolitis in US Undercooked poultry	GBS	2-5d	✓	✓	–	–	✓	–
Salmonella	#2 MCC enterocolitis in US Outbreaks Undercooked egg, dairy, poultry		1-3d	✓	✓	–	–	✓	–
Shigella	Community-acquired, person-to-person		1-3d	✓	✓	✓	–	✓	–
EIEC	Outbreaks Undercooked beef, raw seed sprouts	Produces Shiga toxin	1-8d	–	✓	–	✓	–	✓
C. difficile	Nosocomial	Leukocytosis		–	–	X	–	✓	–
E. histolytica	Travel to tropical regions			–	–	–	–	–	✓
Giardia	Day care, waterborne transmission		1-3d	X	✓	–	X	X	X
Vibrio	Contaminated water, seafood		1-3d	–	–	–	–	–	–
Yersinia	Foodborne transmission	Mesenteric lympadenitis (simulates acute appendicitis)	1-3d	✓	✓	–	–	–	–

References:

Huilan, S., Zhen, L. G., Mathan, M. M., Mathew, M. M., Olarte, J., Espejo, R., Khin Maung, U., et al. (1991). Etiology of acute diarrhoea among children in developing countries: a multicentre study in five countries. Bulletin of the World Health Organization, 69(5), 549–555.
Navaneethan, U., & Giannella, R. A. (2008). Mechanisms of infectious diarrhea. Nature clinical practice. Gastroenterology & hepatology, 5(11), 637–647. doi:10.1038/ncpgasthep1264
Steiner, M. J., DeWalt, D. A., & Byerley, J. S. (2004). Is this child dehydrated? JAMA : the journal of the American Medical Association, 291(22), 2746–2754. doi:10.1001/jama.291.22.2746
Gorelick, M. H., Shaw, K. N., & Murphy, K. O. (1997). Validity and reliability of clinical signs in the diagnosis of dehydration in children. Pediatrics, 99(5), E6.
Harris, JB, Pietroni M. Approach to the child with acute diarrhea in developing countries. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
Thielman, N. M., & Guerrant, R. L. (2004). Clinical practice. Acute infectious diarrhea. The New England journal of medicine, 350(1), 38–47. doi:10.1056/NEJMcp031534

A System for Differential Diagnosis

Given the objective of this site – namely to approach the evaluation of patients in a systematic fashion – I thought it would be useful to put some thought into how best to develop these systems. The method I’ll detail below might be cumbersome to apply in every situation, but (at this point at least) it is the best way to ensure that nothing is overlooked.

A System for Differential Diagnosis:

Any illness or abnormality for which a patient could seek medical attention (or a colleague, consultation) can be broadly encompassed by the statement above. The differential diagnosis is developed by delineating the chief concern(s) or primary aberrant signs, and selecting a relevant mixture of disease processes and organ systems. The differential can be narrowed by determining subjective and objective details surrounding the chief concern. The differential can be broadened by expanding each major category into subcategories.

References:

Benbassat, J., & Bachar-Bassan, E. (1984). A comparison of initial diagnostic hypotheses of medical students and internists. Journal of medical education, 59(12), 951–956.
Bowen, J. L. (2006). Educational strategies to promote clinical diagnostic reasoning. The New England journal of medicine, 355(21), 2217–2225. doi:10.1056/NEJMra054782
Coderre, S., Mandin, H., Harasym, P. H., & Fick, G. H. (2003). Diagnostic reasoning strategies and diagnostic success. Medical education, 37(8), 695–703.
Fulop, M. (1985). Teaching differential diagnosis to beginning clinical students. The American journal of medicine, 79(6), 745–749.
Graber, M. L., Tompkins, D., & Holland, J. J. (2009). Resources medical students use to derive a differential diagnosis. Medical teacher, 31(6), 522–527.
Sapira, J. D. (1981). Diagnostic strategies. Southern medical journal, 74(5), 582–584.

Gastosin Ingestion

CC:

“Gastosin” ingestion

HPI:

29F BIB family after patient was found down at home, near opened bottle of Gastosin in presumed suicide attempt. On arrival to ED, patient was awake, but unresponsive, groaning and clutching stomach. GCS was E3-V2-M5, HR 110, BP 60/palp, RR 24.

ED Course:

Upon arrival, placed two large-bore IV w/rapid infusion of 2L NS and given DA 2g IV x2. NG tube placed, initiated lavage of gastric contents with NS. Patient’s mental status continued to deteriorate, became unresponsive.

PMH/PSH:

Unknown

SHx:

History of alcohol abuse and depression per family.

PE:

VS: 110bpm, 60/palp, 24 R/min, no temp/O2sat available
General: Ill-appearing female, laying on bed in considerable distress, groaning and clutching stomach, diaphoretic
HEENT: NC/AT, PERRL (4-3mm), EOMI, MMM no lesions, no tongue lacerations, breath with foul odor, TM’s clear b/l.
CV: RRR, normal S1/S2, tachycardia, faint heart sounds, JVP elevated though patient supine
Lungs: CTAB, no crackles/wheezes
Abdomen: +BS, soft, non-distended, no guarding, no ecchymosis
GU: Normal external genitalia, loss of stool noted.
Neuro: Patient confused, initially responsive to sternal rub, moving all 4 extremities spontaneously/equally, EOMI without nystagmus, gag reflex present, DTR 2+ and symmetric throughout with toes downgoing.
Extremities: Cool, peripheral pulses 0 (radial, PT, DP), 1+ (femoral, brachial, carotid)¹, capillary refill 3sec
Skin: No visible skin lesions

Assessment & Plan:

29F, unknown PMH, ċ ingestion of unknown amount of “Gastosin”. Patient presenting in likely cardiogenic shock given hypotension with reflex sympathetic activation (evidenced by peripheral vasoconstriction à cool extremities, diaphoresis) and no evidence of hemorrhage. Gastosin is a pesticide used in the storage of maize², and is well-known locally as a common agent in self-poisonings. Chemically composed of aluminum phosphide, and liberates phosphine gas on exposure to moisture which is rapidly absorbed by inhalation, transdermally or gastrointestinally. Toxicity results from free radical damage and inhibition of enzymes of metabolism (particularly affecting cardiac myocytes). Clinical features include vomiting, resistant hypotension and metabolic acidosis.³

Patient’s symptoms and presentation are consistent with cardiogenic shock secondary to Gastosin ingestion. Management included fluid resuscitation and inotropic support with dopamine, as well as gastric lavage. Resuscitation efforts were unsuccessful and patient remained hypotensive with worsening of mental status, and eventual death.

Differential Diagnosis for Shock:

A System for the Management of Aluminum Phosphide Poisoning:^4,5

The Glasgow Coma Scale:

	Eye Opening	Best Motor Response	Best Verbal Response
1	None	None	None
2	Pain	Extension	Groans
3	Verbal	Flexion	Unintelligible
4	Open	Withdraws	Disoriented
5		Localizes	Oriented
6		Obeys commands

References:

Hill RD, Smith RB III. Examination of the Extremities: Pulses, Bruits, and Phlebitis. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 30. Available from: http://www.ncbi.nlm.nih.gov/books/NBK350/
Udoh, J., Ikotun, T., & Cardwell, K. (n.d.). Storage systems for maize (zea mays l.) in nigeria from five agro-ecological zones. Proceedings of the 6th International Working Conference on Stored-product Protection, 2, 960-965.
Bogle, R. G., Theron, P., Brooks, P., Dargan, P. I., & Redhead, J. (2006). Aluminium phosphide poisoning. Emergency medicine journal : EMJ, 23(1), e3. doi:10.1136/emj.2004.015941
Gurjar, M., Baronia, A. K., Azim, A., & Sharma, K. (2011). Managing aluminum phosphide poisonings. Journal of Emergencies, Trauma, and Shock, 4(3), 378–384. doi:10.4103/0974-2700.83868
Jones, A. L., & Volans, G. (1999). Management of self poisoning. BMJ (Clinical research ed.), 319(7222), 1414–1417.

Skull Fracture

$Frontal bone fracture$ ID:

14 year-old female, previously healthy, brought in by ambulance s/p auto vs. pedestrian.

HPI:

Incident unwitnessed, paramedics report no LOC with GCS 15 at scene. GCS 10 upon arrival to ED, with 2min GTC seizure. Patient intubated for airway protection and CT head showed non-displaced frontal bone fracture and small frontal SAH. Patient self-extubated, returned to baseline mental status and was transferred to PICU.

PE:

VS: 128/76mmHg, 120bpm, 22 R/min, 100% RA, 37.6°C
General: Alert and responsive young female with multiple bandages on extremities
HEENT: Right frontal hematoma, no bony defect palpated, multiple facial abrasions, no otorrhea, no rhinorrhea, TM clear b/l, no other ecchymosis.
CV: RRR, normal S1/S2, no M/R/G
Lungs: CTAB
Abdomen: +BS, soft, NT/ND, no rebound/guarding, no flank ecchymoses
Neuro: AAOx3, CN II-XII intact, sensation/motor/reflexes symmetric and intact.
Extremities: Well-perfused with good pulses, no focal bony tenderness, no joint effusions, multiple abrasions on extensor surfaces of all four extremities.

Assessment & Plan:

14yo female, previously healthy, s/p auto vs. peds followed by GTC seizure and CT head showing small SAH and non-displaced frontal bone skull fracture. No evidence of basilar skull fracture on examination or imaging. Seizure likely 2/2 irritation from SAH. Patient was followed closely in PICU with q1h neuro checks with low threshold for repeat CT if change in mental status or more seizures occurred. The patient was eventually transferred to the general ward and was discharged with neurology follow-up and Keppra for seizure prophylaxis for 6mo.

Types of Skull Fractures:

$A system for skull fractures$

Failure to Thrive

ID:

5mo female with a history of multiple food allergies, GERD and FTT admitted from clinic for persistent failure to gain weight.

HPI:

The patient’s mother states that the current diet is 3oz of Neocate 20cal/oz q3h, and that the baby sleeps through the night. The child has a history of reflux, but no emesis in the past few weeks since starting Reglan. There was a history of bloody diarrhea, however none since age 2mo after a change of formula. Mother reports known allergies to milk, soy, protein, and egg. No recent fevers/chills, emesis, diarrhea, fussiness.

The patient was born at 27wks via emergency Cesarean for non-reassuring fetal heart tracings, was intubated in the DR and remained in the NICU for one week.

PE:

VS: 98/65mmHg, 114bpm, 98.1°, 33/min, 100% RA
Gen: Small for age, smiling and interactive
HEENT: PERRL, MMM, no lesions
CV: RRR, no M/R/G, Lungs: CTAB
Abdomen: +BS, soft, NT/ND, no masses, no hepatosplenomegaly
Ext: Normal capillary refill

Assessment & Plan:

5mo female, ex-27wks with a history of multiple food allergies, GERD, FTT. Persistent failure to gain weight, admitted for evaluation of feeding habits and observed weight gain. The patient was determined to not be receiving adequate intake and was advanced to a high-calorie formula and parental education was provided. After two days of observed (and appropriate) weight gain, the patient was discharged with follow-up at multiple specialty clinics including GI, FTT, and A&I.

Differential Diagnosis for Failure to Thrive:

Quick Case: Pleuritic Chest Pain

30yo male presenting with forearm cellulitis, also complaining of right-sided sharp chest pain worse with deep inspiration and some movements of the ipsilateral shoulder. Found to have multiple pulmonary nodules (suggestive of metastasis) with the largest being a subpleural nodule in the superior/anterior portion of the RUL (roughly the location of the patient’s pain).

Differential Diagnosis of Pleuritic Chest Pain

Location of Referred Pain

Sore Throat

ID:

17 year-old female presenting to the pediatric ED with sore throat for 2 days.

HPI:

The patient reports steadily worsening sore throat over the past 2 days, associated with a sensation of swelling. The pain is described as sharp, 4/10 in severity, located on the left side of her throat, and worsened with swallowing. She denies inability to swallow or difficulty breathing, she also denies fever, cough, new skin rashes or genital lesions.

She has no PMH/PSH, takes no medications, denies t/e/d use and is not currently sexually active.

PE:

VS: 111/65mmHg, 80bpm, 97.8°, 16/min, 100% RA
Gen: Well-appearing, NAD
HEENT: PERRL, no conjunctival injection, TM clear b/l, minimal pharyngeal erythema on left with 6mm white circular lesion on left tonsil, no tonsillar enlargement, no uvular deviation, no cervical LAD, neck supple no masses, normal neck ROM
CV: RRR, no M/R/G, Lungs: CTAB
Abdomen: +BS, soft, NT/ND
Ext: Warm, well-perfused, normal peripheral pulses

Assessment & Plan:

17yo female with no significant PMH with acute pharyngitis for 2 days. The most likely cause of the patient’s symptoms is viral pharyngitis, potentially herpangina (given the appearance of the tonsillar lesion). A more serious viral/bacterial pharyngitis is less likely given the absence of fever or significant erythema/exudate. There was no uvular deviation to suggest peritonsillar abscess and no evidence of airway obstruction to suggest other acute processes (epiglottitis, retropharyngeal abscess). The plan is to recommend supportive care and ibuprofen for symptomatic relief. The patient will be discharged home in good condition with precautions to return if symptoms worsen or she begins to have difficulty swallowing/breathing.

Differential Diagnosis of Acute Pharyngitis:

Evaluation (history):

Respiratory distress: epiglottitis, retropharyngeal abscess, peritonsillar abscess, EBV (obstruction in or near pharynx)
Fatigue: infectious mononucleuosis
Abrupt onset: epiglottitis

Evaluation (physical examination):

Vesicles anterior: herpetic stomatitis, SJS, Behcet
Vesicles posterior: herpangina (± involvement of extremities)
Asymmetry: peritonsillar abscess
Stridor, drooling, respiratory distress: airway obstruction
Generalized inflammation: Kawasaki

Pediatric Fever

ID:

5yo girl brought to the pediatric emergency department by her mother due to 3 days of fever.

HPI:

The patient’s fever was first noted 3 days ago, measured at home to 103°F. It is associated with a moist cough, vomiting, and decreased PO intake. Her mother reports that she appears lethargic and has been urinating less frequently. The patient denies headache, changes in vision, burning with urination, or ear pain. No known sick contacts, attends day care.

PMH (Birth History):

No significant medical/surgical history. Ex-term born NSVD with no complications.

PE:

VS: 95/65mmHg, 100bpm, 102.6°, 22/min
General: Well-appearing, mildly irritated but consolable
HEENT: NC/AT, PERRL, oropharynx without erythema, no cervical LAD
CV: RRR, no M/G/R
Lungs: No evidence of respiratory distress (retractions, flaring), faint crackles over right inferior lung fields
Abd: +BS, soft, non-distended, TTP RLQ > LLQ, no rebound/guarding
Back: No CVAT

Labs/Imaging:

CXR PA/Lateral: RML/RLL infiltrate

Assessment:

5yo with 3 days persistent high fever and cough. These symptoms along with examination findings of crackles warranted further imaging (CXR) which revealed infiltrate in the right inferior lung field. The patient appeared clinically stable and was tolerating PO intake in the ED and was discharged home with azithromycin 5mg/kg/dose (with loading dose), clinic follow-up and strict return precautions.

Evaluation and Management of Pediatric Fever

A System for Pediatric Fever:

Pathophysiology:

Diagnosis:

<3mo: 38.0°C, 100.4°F
3-36mo: 39.0°C, 102.2°F
Rectal > oral > axillary

Differential Diagnosis of Pediatric Fever:

Serious Bacterial Illness (SBI):

1) UTI and pyelonephritis

Most common cause of SBI
Accounts for 3-8% of uncharacterized fevers
Female > male, uncircumcised > circumcised
Consider BCx, CSF evaluation as 5-10% bacteremic at presentation
Urinalysis: LE 75% specificity, Nitrites 97% specificity

2) Pneumonia and sinusitis

Sinusitis uncommon <3yo (sinuses unformed)
PNA diagnosed with CXR, obtain if findings of respiratory distress (grunting, tachypnea, hypoxemia) or rales on exam

3) Meningitis

Diagnose with LP
Meningitis suggested if:
- ANC > 1,000
- Protein > 80
- Seizure (particularly complex febrile seizure)

Diagnosis by Age Group:

<3mo

Physical exam findings:
- Tachypnea, hypoxemia → LRT infection
- Irritability, inconsolability, bulging anterior fontanelle → meningitis
- Vomiting/diarrhea → non-specific, GE, AOM, UTI, meningitis
History
- Recent immunization: increased risk of SBI (usually UTI) 24-72h after immunization
- Confirmed bronchiolitis (viral): enterovirus/parainfluenza associated with SBI

3-36mo

Physical exam findings:
- Viral (URTI, GE) → vomiting, diarrhea, rhinorrhea, cough, rash; still playful and responsive
- UTI → fever, foul-smelling urine, crying when urinating
- Meningitis → irritability with handling, vomiting, bulging anterior fontanelle, complex febrile seizures

>36mo

Physical exam findings: presentation more adult-like
Watch for:
- Group A Streptococcal pharyngitis
- Infectious mononulceosis
- Kawasaki: high fever (>5d), strawberry tongue, conjunctivitis, desquamating rash on palms/soles

External Links

WikEM: Pediatric fever of uncertain source

Acute Pelvic Pain

ID:

19yo G0, hCG negative, presenting with lower abdominal pain for 3 weeks.

HPI:

The patient states that she has had progressively worsening lower abdominal pain for the past three weeks. She describes the pain as constant, cramping, currently 8/10 in severity with radiation to the right flank. The pain is improved somewhat with ibuprofen and worsened with movement. She reports subjective F/C, some vaginal bleeding, but no other discharge and no dysuria. She is sexually active with one partner, using condoms occasionally. She has no significant PMH, no history of STI and a PSH of appendectomy. She denies any current or prior T/E/D use.

PE:

VS: 110/60mmHg, 60bpm, 99.5°, 16/min
HEENT: NC/AT, PERRL, EOMI, MMM w/o lesions
CV: RRR, no M/G/R
Lungs: CTAB
Abd: +BS, soft, non-distended, TTP RLQ > LLQ, no rebound/guarding
Back: no CVAT
Pelvic: external genitalia normal, scant blood in vault, os closed, no discharge, + CMT, + uterine tenderness, + adnexal tenderness

Labs/Imaging:

TVUS: normal appearing uterus/adnexa, possible free fluid (hemorrhagic vs. inflammatory) in pelvis
Wet mount: negative
Urine dip: -LE/nitrites, -protein, +blood

Assessment:

19yo G0, hCG negative, with pelvic pain and vaginal bleeding. Findings of lower abdominal tenderness, cervical motion/uterine/adnexal tenderness on examination, and low-grade fever are suggestive of PID. Other considerations include UTI, however, absence of dysuria, CVAT, and negative urine dip do not support this diagnosis. Will evaluate further with GC/CT, and treat empirically with ceftriaxone 250mg IM x1 and doxycycline 100mg PO BID x14d with follow-up in 48h.

Differential Diagnosis of Acute Pelvic Pain:

Common causes:

Gynecologic
- PID, TOA
- Neoplasm (torsion, rupture)
- Leiomyoma (torsion, degeneration)
- Endometriosis
- Endometritis
- Ectopic pregnancy
- SAB
Obstetric
- Labor
- Uterine rupture
- Abruptio placentae
- Diastasis symphesis pubis
Non-gynecologic
- Appendicitis
- Cystitis (UTI)
- Diverticulitis
- Urinary tract calculi
- Abdominal wall trauma

Location of pain:

ROS:

discharge + dyspareunia: PID
missed menses + cramping/bleeding: SAB, ectopic
anorexia, N/V: appendicitis, torsion

A System for the Evaluation and Management of PID:

Pathogens: GC, CT, gardnerella, haemophilus
Evaluation:
- Pelvic exam: CMT, uterine tenderness, adnexal tenderness, abnormal discharge, wet mount WBC’s
- Labs: + GC/CT, ↑ ESR/CRP
- VS: T > 101°
- Imaging: thickened tubes, free pelvic fluid, TOA
Indications for admission:
- Acute abdomen, toxic appearance, unstable VS
- Pregnancy
- Failed outpatient, can’t tolerate PO
- TOA
Outpatient management:
- Ceftriaxone 250mg IM x1
- Doxycycline 100mg PO BID x14d
- ± Metronidazole 500mg PO BID x14d

References:

Hacker and Moore’s essentials of obstetrics and gynecology. Philadelphia, PA: Saunders/Elsevier, 2010.
CDC – Pelvic Inflammatory Disease – 2010 STD Treatment Guidelines: http://www.cdc.gov/std/treatment/2010/pid.htm

3rd Trimester Bleeding

ID:

A 34yo G4P2011 at 32w3d by LMP = 2nd trimester ultrasound with a history of GDMA1 is BIB ambulance for vaginal bleeding.

HPI:

She states that she awoke at 0230 that morning noting significant vaginal bleeding. She denied any associated abdominal pain, uterine contractions, leakage of fluid or other vaginal discharge and has continued to note fetal movement. Her current pregnancy has been uncomplicated though she reports mention of a “low placenta”.

PE:

VS: 115/80mmHg, 90bpm, 98.1°, 18/min, 99%
Gen: Appears distressed
HEENT: PERRL, EOMI, MMM, no conjunctival pallor
CV: RRR, no M/R/G, Lungs: CTAB
Abdomen: gravid (FH 30cm), +BS, NT, no rebound/guarding
SSE: os closed, no motion tenderness, several large clots removed from vault

Imaging/Studies:

NST: baseline 140bpm, moderate variability, accelerations, no decelerations
U/S: AFI 10.6, placenta entirely covering internal os

Assessment & Plan:

34yo G4P2011 at 32w3d by L=2 with complete placenta previa confirmed by TVUS presenting with first episode of vaginal bleeding.

Differential Diagnosis of 3rd Trimester Bleeding:

References:

Sakornbut, E., Leeman, L., & Fontaine, P. (2007). Late pregnancy bleeding. American family physician, 75(8), 1199–1206.

Syncope

ID:

A 50 year-old male with a reported two-year history of infrequent spells, presenting with two spells in the past two days.

HPI:

The patient’s spells began two years ago, he recounts that he was watching television when he lost consciousness and a friend noted he started shaking; he does not recall the event, and awoke in the hospital. The next spell occurred one year later, though the patient is unable to recall much about this episode. The patient remained spell-free until yesterday when he was on a bus, lost consciousness and awoke in a hospital. He notes that he had bit his tongue and lost control of his bladder. He was discharged hours later with a prescription for an AED which he was unable to fill. This morning, the patient had another spell while in the bathroom. His roommate heard him fall, found him on the ground, and noted that his mouth was moving but did not see any other movements.

The patient’s episodes are all associated with loss of consciousness and are followed by 5-10 minutes of disorientation after which he recovers fully. The episodes are sometimes preceded by a feeling of “euphoria”, though this feeling sometimes occurs without subsequent LOC.

The patient denies any associated palpitations, dizziness/LH, chest pain or muscle pain. He has not had any recent fevers/chills, dysuria, cough, headache, changes in vision, numbness/tingling, weakness, difficulty speaking or swallowing or weight loss. He also denies any history of head trauma.

Physical Examination:

VS: Stable and WNL
General: Well-appearing, pleasant, and in NAD.
HEENT: NC/AT. MMM. Small lesion on tongue.
Lungs: CTAB.
CV: RRR with occasional ectopic beats, no M/R/G.
Abdomen: S/NT/ND. Bowel sounds present.
Neurological exam: AAOx4, CN II-XII intact, motor/sensation/reflexes/coordination/gait WNL

Imaging/Studies:

EKG: Occasional PAC/PVC
CT Brain: Unremarkable except for mild age-related cerebral atrophy

Assessment & Plan:

50 year-old male with a history of HTN and a reported two-year history of infrequent spells presenting with two spells in the past two days. The description of the patient’s episodes could be consistent with seizures. Aspects supporting this notion include loss of consciousness and period of confusion following each episode. One of the recent episodes was also associated with tongue-biting and loss of bladder control. Additionally, some episodes are associated with a sensation of euphoria rising from the abdomen to the head which could be indicative of an aura. Characteristics that suggest other causes include the absence of noted convulsions and non-stereotyped nature of each episode which could be due to the patient’s poor recollection of these events and absence of reliable witnesses. In the case of true seizures, the possible etiologies in this patient include a mass, metabolic abnormalities, substance use, or concomitant infection exacerbating an existing propensity for seizure activity. Other, non-seizure causes warranting evaluation include cardiogenic syncope particularly given the evidence of ectopic beats on examination and electrocardiogram.

Differential Diagnosis of Syncope

First, is it syncope? History is very important for distinguishing syncope from other causes (seizure, dizziness, vertigo, presyncope). Ask about precipitating events, prodromal symptoms, post-ictal confusion. Common causes of syncope and their associated symptoms are detailed in the figure below.

References:

Kapoor, W. N. (2000). Syncope. The New England journal of medicine, 343(25), 1856–1862. doi:10.1056/NEJM200012213432507

Causes of an Elevated Hemidiaphragm

References:

CC:

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs:

Imaging:

Pleural Effusion

Cirrhosis and Portal Hypertension

SMV Thrombosis

B/L Inguinal Hernias

Large Right Inguinal Hernia

CT Abdomen/Pelvis (PVT)

Assessment/Plan:

Renal Failure in Cirrhosis:

Pathophysiology of Hepatorenal Syndrome:

Evaluation:

Treatment:

Summary:

References:

CC:

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Assessment/Plan:

Differential Diagnosis of Macroscopic Hematuria

Important Historical Elements:

Guided Lecture

References:

CC:

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs:

Studies:

Assessment/Plan:

Imaging:

ERCP

MRCP

CT Abdomen/Pelvis

Differential Diagnosis of Hyperbilirubinemia: 1, 2

Evaluation of Hyperbilirubinemia: 3

References:

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs:

Studies:

Assessment/Plan:

Differential Diagnosis of Nausea/Vomiting: 1, 2

Pathophysiology: 3, 4, 5

Important history/physical associations: 4

Differential Diagnosis of Abdominal Pain By Location:

References:

CC:

HPI:

PMH:

PSH:

FH:

Differential Diagnosis of Hyperbilirubinemia: ^{1, 2}

Evaluation of Hyperbilirubinemia: ³

Differential Diagnosis of Nausea/Vomiting: ^{1, 2}

Pathophysiology: ^{3, 4, 5}

Important history/physical associations: ⁴

Differential Diagnosis of Hemoptysis: ^{2, 3}

A System for the Diagnosis of Tuberculosis: ^{4, 5}

A System for Vasculitides: ^{8, 9}

Vasculitis Mimics: ⁹

Interpretation of antineutrophil cytoplasmic autoantibodies (ANCA): ¹⁰

Differential Diagnosis of Anemias: ¹¹

Differential Diagnosis for bowel obstruction: ^{1, 2, 3}

Types of Abdominal Pain: ⁴

Physical Examination Techniques: ¹

Types of Abdominal Wall Hernias: ²

Differential diagnosis for groin masses: ⁴

Locations of Groin Masses: ⁹