Acute Diarrhea (in developing countries)

A clinic near JalapaHPI:

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

Types and Causes of Acute Diarrhea

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

Management of Acute Diarrhea

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:

  1. 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.
  2. Navaneethan, U., & Giannella, R. A. (2008). Mechanisms of infectious diarrhea. Nature clinical practice. Gastroenterology & hepatology, 5(11), 637–647. doi:10.1038/ncpgasthep1264
  3. 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
  4. 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.
  5. Harris, JB, Pietroni M. Approach to the child with acute diarrhea in developing countries. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
  6. 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:

A system for systems

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:

  1. 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.
  2. 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
  3. Coderre, S., Mandin, H., Harasym, P. H., & Fick, G. H. (2003). Diagnostic reasoning strategies and diagnostic success. Medical education, 37(8), 695–703.
  4. Fulop, M. (1985). Teaching differential diagnosis to beginning clinical students. The American journal of medicine, 79(6), 745–749.
  5. Graber, M. L., Tompkins, D., & Holland, J. J. (2009). Resources medical students use to derive a differential diagnosis. Medical teacher, 31(6), 522–527.
  6. Sapira, J. D. (1981). Diagnostic strategies. Southern medical journal, 74(5), 582–584.

Gastosin Ingestion

Jalapa, NicaraguaCC:

“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 Shock

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

Management of Aluminum Phosphide Poisoning

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:

  1. 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/
  2. 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.
  3. 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
  4. 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
  5. Jones, A. L., & Volans, G. (1999). Management of self poisoning. BMJ (Clinical research ed.), 319(7222), 1414–1417.

Skull Fracture

Frontal bone fractureID:

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

Failure to ThriveID:

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:

A System for Failure to Thrive

 

Quick Case: Pleuritic Chest Pain

Image from: Maeng, C. H., Chin, S. O., Yang, B. H., Kim, S.-Y., Youn, H.-J., Cho, K. S., Baek, S. K., et al. (2007). A case of organizing pneumonia associated with rituximab. Cancer research and treatment : official journal of Korean Cancer Association, 39(2), 88–91. doi:10.4143/crt.2007.39.2.88

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

Causes of Pleuritic CP

Location of Referred Pain

Referred Pain

 

Sore Throat

Oropharynx AnatomyID:

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:

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

CXR with infiltrates

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

Algorithm for the Evaluation of Pediatric Fever

A System for Pediatric Fever:

Pathophysiology:

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:

Causes Of 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

Acute Pelvic Pain

Pelvic US - free fluidID:

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:

LocationOfPain

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:

  1. Hacker and Moore’s essentials of obstetrics and gynecology. Philadelphia, PA: Saunders/Elsevier, 2010.
  2. 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:

  1. 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:

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

Delirium

ID:

A 70 year-old female with a PMH of HTN, DM, hyperlipidemia and stage I breast cancer s/p lumpectomy with sentinel LN biopsy several years ago presented for elective surgery complicated by post-operative bleeding. She is now 4 days post-op and was found to be confused, somnolent and occasionally agitated.

HPI:

The patient could not be interviewed.

PE:

  • VS: Stable and within normal limits
  • General: unremarkable except for crackles in bilateral lung bases
  • MSE: only arouses to sternal rub and becomes agitated, moving all four extremities spontaneously and symmetrically.
  • Reflexes: corneal and gag reflexes present, suppresses eye movements with head turn, deep tendon reflexes 3+ throughout UE/LE bilaterally.

Assessment:

70 year-old woman with a history of HTN, DM, hyperlipidemia and breast cancer presents with worsening confusion, somnolence and occasional agitation four days after surgery. The combination of significantly altered consciousness and absence of focal neurological findings, all in the setting of a complicated surgical course suggest delirium.

Differential Diagnosis of Altered Mental Status:

Levels of consciousness

There are different levels of consciousness, they are named in the diagram below but are better described by the characteristics observed.

Initial assessment

Differential Diagnosis for Altered Mental Status

References:

  1. Inouye, S. K. (2006). Delirium in Older Persons. The New England journal of medicine, 354(11), 1157–1165. doi:10.1056/NEJMra052321
  2. Blueprints neurology. Philadelphia: Wolters Kluwer Health/Lippincott William & Wilkins, 2009.
  3. Tindall SC. Level of Consciousness. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 57. Available from: http://www.ncbi.nlm.nih.gov/books/NBK380/

Headache, vertigo and weakness

ID:

30 year-old male with no significant PMH presenting with right-sided “weakness”, vertigo and headache for three days.

HPI:

The patient was in his normal state of good health until three days prior to admission when he was out shopping and felt a headache and right-sided weakness. The headache came on suddenly, felt “sharp”, 7/10 in severity and radiated from the posterior occiput to his forehead on the right side. The headache was associated with vertigo and nausea/vomiting. At the same time, the patient noticed that he was no longer able to walk, describing “weakness” on the right side. He also began feeling dizzy, describing the sensation as “room spinning”. He denied changes in vision, hearing, difficulty speaking or swallowing (though he has had persistent hiccups for the past few days). He also denied CP, palpitations, SOB. He did seek immediate medical attention at an OSH but is unable to recall what was done and he was discharged from the ER on the same day. He presents 3 days later with persistent symptoms.

PE:

  • Mental status: normal
  • CN II-XII: intact with the exception of decreased sensation to sharp touch on right face and decreased gag reflex
  • Motor: normal bulk/tone, strength 5/5 in UE/LE bilaterally
  • Sensory: decreased sensation to pain and temperature on left body
  • Gait: wide-based, unable to tandem, heel, toe walk. Walking in place, he turns to the right.

Assessment:

30 year-old male with no PMH presenting with 3 days of HA, vertigo, hiccups, right-sided ataxia, and alternating decreased pain and temperature sensation on ipsilateral face and contralateral hemibody. These symptoms are suggestive of a brainstem lesion, localizing to the medulla. Hiccups suggest involvement of nucleus ambiguus (CN IX, X, XII). Alternating decreased pain/temperature sensation suggests involvement of the spinal tract of CN V, and interruption of fibers of the descending spinothalamic tract. These findings point further to a lesion in the right lateral medulla, likely vascular given the rapid onset of symptoms. Associated findings of right-sided ataxia suggests involvement of the superior cerebellar peduncle (restiform body) in the posterior lateral medulla. An MRI brain showed the lesion shown in Fig-1, and a CTA head/neck the following day showed dissection of the right vertebral artery.

A System for Cerebrovascular Disease:

Types of strokes

Clinical characteristics of strokes

Strokes are characterized by the sudden onset of focal neurological deficits. These are typically unilateral and consciousness is generally maintained.

  • dysphasia
  • dysarthria
  • weakness
  • ataxia
  • sensory loss
  • neglect
  • hemianopsia

If some of these typical features are not present (ex. gradual onset, significantly impaired consciousness, seizures early), consider alternative diagnoses (ex. hypoglycemia, subdural hematoma, mass, postictal paresis, migraine).

Common causes of stroke

The most common causes are atherosclerosis (leading to thromboembolism or local occlusion) and cardioembolism. If the patient does not have risk factors, consider alternatives:

  • contralateral ptosis/miosis: carotid artery dissection affecting sympathetic fibers
  • fever + murmur: infective endocarditis
  • HA + ↑ESR: giant-cell arteritis

References:

  1. Agabegi, S. (2013). Step-up to medicine. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins.
  2. van der Worp, H. B., & van Gijn, J. (2007). Acute Ischemic Stroke. The New England journal of medicine, 357(6), 572–579. doi:10.1056/NEJMcp072057

Intro to “DDx of”

I’m a medical student currently rotating through clinical clerkships resident in emergency medicine. The purpose of this website is to force me to learn. Recently, I’ve found it increasingly difficult to study from review books, and even more difficult to recall and apply that information practically. What has been working is reading heavily about specific cases I’ve seen. Having a real person in mind, hearing their complaints, doing their examination and then supplementing the experience with targeted reading sticks far better.

As for the format, something that has been hammered into me over the past year is to be systematic in everything I do. The benefits being that I’m less likely to miss stuff if I approach everything the same way. The other benefit for me is that I find these systems to be a better way to learn. Less mnemonics, more flowcharts.

So, I’ll select appropriate cases I encounter (altering identifying information of course), read into it a bit, and create a systematic approach for the evaluation, diagnosis and management of that chief complaint.

The site’s going to be a bit rough, the goal is to make it easy to quickly archive these experiences for future reference and learning.