Fever

Causes of Fever

Key Features

Morbidity and mortality increase with age and comborbidities
Most common sources in elderly: respiratory, genitourinary, skin/soft-tissue
Atypical presentations: functional decline, altered mental status

Immediate Evaluation and Management

Critical Findings
- Altered mental status
- Respiratory distress
- Hemodynamic instability
Critical Interventions
- Airway management, supplemental O2
- Cardiac monitoring
- Fluid resuscitation
- Empiric antibiotics
- Cooling measures (T>41.0°C)

Pathophysiology of Fever

Production of endogenous or exogenous pyrogens
Increase temperature set point in hypothalamus: Patient experiences chills when core temperature < set point
Vasoconstriction, shivering causes fever: Patient experiences euthermia, though may feel malaise, fatigue
Resolution: Patient experiences sweats until core temperature returns to normal set point

References

Blum, F., & Biros, M. (2013). Fever in the Adult Patient. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 119-123). Elsevier Health Sciences.

ECG Guide

The format of this article is atypical for the structure and concept of the website – but it’s always been about learning. Here is a simplified guide to ECG interpretation with a focus on the aspects I find more challenging to understand or recall.

Grid and Leads

Axis

Atrial Enlargement

Normal:: First portion of deflection is RA, second is LA
Right Atrial Enlargement:: P-wave amplitude > 2.5mm in inferior leads; Normal duration P-wave
Left Atrial Enlargement:: P-wave duration increased (terminal negative portion >0.04s); Amplitude of terminal negative component >1mm below isoelectric line in V1

Ventricular Hypertrophy

Right Ventricular Hypertrophy:

Right axis deviation

Abnormal R-wave progression

Increased R-wave amplitude in leads overlying the right ventricle (V1)
Increased S-wave amplitude in leads overlying the left ventricle (V6)

Criteria

V1: R>S
V6: S>R

Left Ventricular Hypertrophy:

Left axis deviation

Increased R-wave amplitude in leads overlying the LV (I, aVL, V5, V6)

Increased S-wave amplitude in leads overlying the RV (V1)

Criteria:

Precordial Leads
- R-wave in V5/V6 + S-wave in V1/V2 > 35mm
- R-wave in V5 > 26mm
- R-wave in V6 > 20mm
Limb Leads
- R-wave in aVL > 11mm
- R-wave in aVF > 20mm
Combined
- R-wave in aVL + S-wave in V3 > 20mm (F), 28mm (M)

Secondary Repolarization Abnormalities

Downsloping ST-segment depression
Asymmetric T-wave inversion

Bundle Branch Blocks

Left Bundle Branch Block

QRS duration > 0.12s (3 boxes)
Broad or notched R-wave with prolonged upstroke in I, aVL, V5, V6
Associated ST-segment depression and T-wave inversion
Reciprocal changes in V1, V2 (deep S-wave)
Possible LAD

Right Bundle Branch Block

QRS duration > 0.12s (3 boxes)
RSR’ in V1, V2
Reciprocal changes in I, aVL, V5, V6 (deep S-wave)

Hemiblocks

Other Blocks

Non-specific intraventricular conduction delay: QRS >0.10s without BBB
Incomplete BBB: LBBB/RBBB pattern with non-prolonged QRS
Bifascicular block: RBBB + LAFB/LPFB (by axis deviation)

Ischemia and Infarction

Hyperacute T-waves
T-wave inversion: Symmetric, compared to TWI associated with repolarization abnormalities
ST-elevation: Unlike J-point elevation, ST-segment merges with T-wave
Q-waves
1. Duration > 0.04s
2. Amplitude > 1/3 R-wave
3. Normal in aVR

Coronary Artery Territories

Distribution	Coronary Artery	Leads	Reciprocal Changes
1. Inferior	RCA, PDA	II, III, aVF	Anterior, Lateral
2. Lateral	LCx	I, aVL, V5, V6	Inferior
3. Anterior	LAD	V1-V6	Inferior
4. Posterior	RCA	Posterior	Anterior (esp. V1)

External Links

Anemia

HPI

70M with a history of dementia presenting with 3 days of fatigue. The patient was unable to provide detailed history, however family members reported worsening fatigue with the patient requiring assistance with ambulation for several days. The patient was referred from an outside clinic after point-of-care hemoglobin of 6.7. No reported history of anemia, and no history suggestive of obvious external bleeding.

Vital signs stable, tachycardia and tachypnea noted with minimal exertion but saturating well on ambient air and in no acute distress. Examination notable for conjunctival pallor without scleral icterus, systolic flow murmur, brown stool guaiac negative.

CBC with hemoglobin of 7.5 , MCV 80.3 , RDW 22.4 , no leukocytosis and normal platelets. Also noted was an alkaline phosphatase of 828 , normal total and direct bilirubin, and undetectable serum troponin. Chest x-ray showed a possible pleural-based mass.

The patient was transfused two units of PRBC’s and admitted for further evaluation. CT chest/abdomen/pelvis revealed sternal and rib-based pleural soft-tissue mass, prostate mass, pelvic and retroperitoneal lymphadenopathy as well as extensive bony metastatic disease consistent with primary prostate cancer with diffused metastasis. Serum PSA was 2,087 . Iron studies suggested anemia of chronic disease. Reticulocytes were not obtained but may have suggested inadequate production index given extensive bony metastases and possible associated myelosuppression. The patient was symptomatically improved after transfusion and discharged with outpatient follow-up for discussions regarding possible biopsy and treatment.

Images

Areas of pleural thickening. Possible pleural based mass in left mid lung.

CT Chest: Lung Window

Rib-based pleural soft tissue masses.
Large 5.6 x 4.4cm anterior sternal soft-tissue mass.

CT Body: Bone Window

Extensive bony metastatic disease.
Prostate mass, large pelvic and retroperitoneal lymphadenopathy.
Consistent with primary prostate cancer with diffuse metastasis.

Algorithm for the Evaluation of Anemia ^1,2

References:

Zaiden R, Rana F. Evaluation of Anemia. BMJ Best Practice. Oct 2014. http://us.bestpractice.bmj.com/best-practice/monograph/93/overview.html. Last accessed 15 May 2015.
Janz, T. G., Johnson, R. L., & Rubenstein, S. D. (2013). Anemia in the emergency department: evaluation and treatment. Emergency medicine practice, 15(11), 1–15– quiz 15–6.
WiKEM: Anemia

Severe Traumatic Brain Injury

HPI:

34 year-old male brought in by ambulance s/p assault. Field GCS reportedly 7, in trauma bay assessed as E2-V4-M6. Witnessed seizure in CT scanner, resolved with lorazepam. Intubated for airway protection, underwent external ventricular drain placement and transferred to surgical ICU.

Initial imaging revealed bifrontal subdural hematomas and right temporal hemorrhagic contusion with generalized edema. Repeat imaging one hour later showed interval development of large extra-axial hemorrhage overlying the right occipital and parietal lobes (2.2cm), representing subdural or epidural hematoma.

The patient’s ICU course was complicated by continued seizures and refractory elevation in intracranial pressure. A pentobarbital infusion was started and titrated to adequate burst suppression and hyperosmolar therapy with both mannitol and hypertonic saline continued. Additional imaging revealed stable hemorrhage but continued diffuse cerebral edema evidenced by sulcal effacement.

On hospital day 5, examination revealed bilateral fixed and dilated pupils. Imaging revealed effacement of basilar cisterns, pre-pontine cistern, and cisterna magna suggestive of impending/ongoing transtentorial and tonsillar herniation. Pentobarbital was weaned and conventional cerebral angiography as well as cerebral perfusion studies were consistent with brain death.

Images

CT head without contrast one hour after presentation

Large extra-axial posterior hemorrhages. Hemorrhagic contusions in the right frontal and temporal lobes.
The cerebral sulci appear effaced – findings suggest diffuse cerebral edema.
S/p EVD using a right frontal approach.

CT head without contrast on hospital day 5

Interval evidence of global hypoxic/ischemic injury to the brain.
Interval apparent effacement of the basilar cisterns, pre-pontine cistern, and cisterna magna suggesting impending/ongoing downward transtentorial herniation and tonsillar herniation.
Stable supra/infratentorial subdural/epidural hematoma.

Algorithm for the Management of Severe Traumatic Brain Injury^1,2

References

Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care, AANS/CNS, Carney, N. A., & Ghajar, J. (2007). Guidelines for the management of severe traumatic brain injury. Introduction. Journal of neurotrauma, 24 Suppl 1, S1–2. doi:10.1089/neu.2007.9997
Stocchetti, N., & Maas, A. I. R. (2014). Traumatic intracranial hypertension. The New England journal of medicine, 370(22), 2121–2130. doi:10.1056/NEJMra1208708
WikEM: Severe traumatic brain injury

Lactic Acidosis

HPI:

59F with a reported history of congestive heart failure, presenting with intermittent chest discomfort for three days.

She characterized this discomfort as “heartburn”, describing a mid-epigastric burning sensation radiating up her neck, not associated with exertion, lasting 1-2 hours and resolving with antacids. The patient has poor exercise tolerance at baseline and for the past several years has been able to ambulate only short distances around her home, and states that these symptoms have been worsening in the past week. She denies chest pain on exertion, orthopnea or paroxysmal nocturnal dyspnea. She states that she was diagnosed with congestive heart failure five years ago, but was never prescribed medications.

On further questioning, the patient reports several weeks of mouth and lip pain which has limited oral intake, though no dysphagia to solids or liquids. She otherwise denies fevers/chills, abdominal pain, nausea/vomiting, cough, changes in urinary or bowel habits.

In the emergency department, the patient was noted to have an elevated serum troponin, though ECG showed no changes of acute ischemia/infarction.

PMH:

Congestive heart failure

PSH:

None

FH:

Mother with diabetes
Father with MI at age 65

SHx:

4-5 drinks of alcohol/day
No tobacco or drug use

Meds:

None

Allergies:

NKDA

Physical Exam:

VS:	T	37.4	HR	106	RR	18	BP	145/82	O2	100% RA
Gen:	Morbidly obese female, lying in bed, in no acute respiratory distress, speaking in complete sentences.
HEENT:	Dry, cracked lips, slightly erythematous, otherwise moist mucous membranes, poor dentition. Mild scleral icterus. No cervical lymphadenopathy.
CV:	Rapid rate, regular rhythm, normal S1/S2, II/VI systolic ejection murmur at LUSB, no radiation appreciated. No jugular venous distension.
Lungs:	Clear to auscultation in posterior lung fields bilaterally, no crackles appreciated.
Chest:	Well-circumscribed erythematous patch in folds beneath left breast, no underlying fluctuance, no significant tenderness to palpation. On contralateral breast, some hyperpigmentation but no erythema.
Abdomen:	Obese, non-tender, non-distended. Patch of erythema below pannus, mildly tender to palpation.
Ext:	Bilateral lower extremities with marked edema and overlying scaly plaques, some slightly ulcerated weeping serous fluid. Peripheral pulses are difficult to palpate, capillary refill difficult to assess.

Labs/Studies:

CBC: 11.1/11.1/34.5/212 (MCV 114.2)
BMP: 140/4.5/97/20/10/1.14/64
Anion Gap: 23
LFT: AST: 73, ALT: 26, AP: 300, TB: 4.6, DB: 2.1, Alb: 3.0, INR 1.3
BNP: 158
Troponin: 1.284

Sinus tachycardia, LVH, secondary repolarization abnormalities

Imaging:

CT Pulmonary Angiography:
No evidence of central pulmonary embolism, thoracic aortic dissection, or thoracic aortic aneurysm. Evaluation of the peripheral vessels is limited due to motion artifact. No focal consolidation or pneumothorax.

CT Abdomen/Pelvis non-contrast:
No evidence of intra-abdominal abscess or definite source of infection. Marked hepatic steatosis.

CT Lower Extremity non-contrast:
Diffuse circumferential subcutaneous edema involving both lower extremities from the level of the mid thighs distally through the feet. There are bilateral subcutaneous calcifications which are likely venous calcifications in the setting of chronic venous stasis disease. There is some overlying skin thickening.

TTE:
There is moderate concentric left ventricular hypertrophy with hyperdynamic LV wall motion. The Ejection Fraction estimate is >70%. Grade I/IV (mild) LV diastolic dysfunction. No hemodynamically significant valve abnormalities.

US Abdomen:
Hepatomegaly, echogenic liver suggesting fatty infiltration. Moderately blunted hepatic vein waveforms suggesting decreased hepatic parenchymal compliance.

Assessment/Plan:

The patient was admitted to the cardiology service for management of NSTEMI and evaluation of undiagnosed CHF. She was started on a heparin continuous infusion. In addition, a CT pulmonary angiogram was obtained to evaluate for pulmonary embolism as an explanation of her progressive dyspnea on exertion. No PE, consolidation or effusion was identified.

Despite the patient’s reported history of congestive heart failure, there was no evidence that her symptoms were a result of an acute exacerbation with only a mildly elevated BNP but no jugular venous distension or evidence of pulmonary edema. The patient’s significant lower extremity edema was more suggestive of chronic venous stasis.

One notable laboratory abnormality that was explored was her elevated anion gap metabolic acidosis. Studies submitted included serum lactate, salicylates, osmolarity, CK, and urinalysis for ketonuria. This evaluation was notable for an elevated serum lactate of 13.2mmol/L and an arterial blood gas that showed adequate respiratory compensation (and no A-a gradient). Given the patient’s modest leukocytosis (with neutrophil predominance), and tachycardia, the concern for sepsis was increased though the source remained unclear. Prominent possibilities included a skin and soft-tissue infection vs. less likely intra-abdominal source though the patient’s physical examination was not suggestive of a process that would produce such a substantial lactic acidosis. Blood cultures were drawn and the patient was started on empiric antibiotics for the suspected sources. In addition, the patient was cautiously volume resuscitated given her reported history of CHF while pending a transthoracic echocardiogram to evaluate cardiac function. Additional imaging including CT abdomen/pelvis and lower extremities was obtained (though without contrast due to the patient’s recent exposure), and no obvious source was identified.

Over the next two days, the patient’s serum lactate downtrended to normal range, as did the serum troponin. A transthoracic echocardiogram showed an LVEF >70% with mild concentric hypertrophy and diastolic dysfunction. Blood and urine cultures were without growth.

Additional issues managed during the hospitalization included elevated serum transaminases (AST > ALT), conjugated hyperbilirubinemia and evidence of decreased hepatic synthetic function with hypoalbuminemia and elevated INR. Given the patient’s history of EtOH use, as well as other corroborating findings including macrocytic anemia, hypomagnesemia, folate and B12 deficiency, this was attributed to alcoholic hepatitis (discriminant function <32). Infectious hepatitis serologies were negative. The patient was started on nutritional supplements. Finally, the patient persistently complained of lip and oral mucosal pain. Examination was without discrete lesions but some mucosal redness was identified. Despite poor dentition, there was no evidence of abscess and HSV/HIV testing was negative. This was thought to be stomatitis caused by her identified nutritional deficiencies.

Differential Diagnosis of Elevated Serum Lactate ^1,2

Algorithm for Evaluation of Acidemia ^3,4

Algorithm for Evaluation of Alkalemia ^3,4

References:

Fall, P. J., & Szerlip, H. M. (2005). Lactic acidosis: from sour milk to septic shock. Journal of intensive care medicine, 20(5), 255–271. doi:10.1177/0885066605278644
Luft, F. C. (2001). Lactic acidosis update for critical care clinicians. Journal of the American Society of Nephrology : JASN, 12 Suppl 17, S15–9.
Ingelfinger, J. R., Berend, K., de Vries, A. P. J., & Gans, R. O. B. (2014). Physiological Approach to Assessment of Acid–Base Disturbances. The New England journal of medicine, 371(15), 1434–1445. doi:10.1056/NEJMra1003327
Ingelfinger, J. R., & Seifter, J. L. (2014). Integration of Acid–Base and Electrolyte Disorders. The New England journal of medicine, 371(19), 1821–1831. doi:10.1056/NEJMra1215672

Pleural Effusion

HPI:

64F with a history of CAD, MI, CHF, CLL and rheumatoid arthritis who presented to the emergency department after transfer from a rehabilitation facility for respiratory distress. The patient reported several days of progressive shortness of breath with dyspnea on exertion. She also noted some associated orthopnea and lower extremity edema. The patient was recently hospitalized for similar symptoms and was diagnosed with CHF at the time. At the rehab facility, the patient became hypoxemic and hypertensive, reporting shortness of breath and chest pain prior to presentation.

Hospital Course:

The patient was initially managed with BiPAP and nitroglycerin continuous infusion, but was then stable on supplemental O2 via nasal cannula and was transitioned to long-acting nitrates and anti-hypertensives. The patient’s hypoxemic respiratory failure was initially attributed to acute exacerbation of left-ventricular heart failure, and the patient was managed with spot diuresis. However, there was no symptomatic improvement and the patient became hypernatremic so diuresis was held as alternative diagnoses were explored.

A transthoracic echocardiogram showed preserved LVEF (50-55%), but some diastolic dysfunction and elevated PAP/RAP. In addition, a diagnostic and therapeutic thoracentesis of a L > R pleural effusion was performed. Pleural fluid studies were suggestive of a transudative process, though with some abnormal characteristics (including lymphocyte predominance, as well as presence of signet cells).

Rheumatology and pulmonology services were consulted for input and recommendations for further evaluation were appreciated. Per rheumatology, the patient’s diagnosis of rheumatoid arthritis may not be consistent with her presentation or prior serologic studies. Her pleural fluid analysis was also not consistent with rheumatoid disease. According to pulmonary consult, the patient’s hypoxemia remains most consistent with left ventricular dysfunction though primary pulmonary processes cannot be excluded (and would warrant further evaluation with imaging and pulmonary function testing).

PMH:

CHF
CAD
CVA
Myocardial Infarction
HTN
Hypothyroidism
CLL
Anemia

PSH:

TAH-BSO

FH:

No family history of autoimmune disease.
Mother: DM

SHx:

Denies tobacco/EtOH/drug use
Lives at home, at SNF since discharge

Meds:

Furosemide 20mg p.o. daily
Gabapentin 300mg p.o. t.i.d.
Hydralazine 50mg p.o. t.i.d.
Hydrochlorothiazide 25mg p.o. b.i.d.
Hydroxychloroquine 200mg p.o. daily
Levothyroxine 25mcg p.o. daily
Minoxidil 2.5mg p.o. b.i.d.
Pantoprazole 40mg p.o. daily
Prednisone 15mg p.o. daily

Allergies:

Shellfish

Physical Exam:

VS:	T	37.2	HR	84	RR	15	BP	147/75	O2	97% 4LNC
Gen:	Elderly female, alert and oriented to self and place, responding appropriately to questions.
HEENT:	Mucous membranes moist, sclera anicteric, no cervical lymphadenopathy.
CV:	Regular rate and rhythm, normal S1/S2, no additional heart sounds. III/VI mid-systolic murmur heard best at LLSB with diastolic component, no radiation appreciated. Non-displaced PMI. JVP measured to 14cm.
Lungs:	Decreased breath sounds in left lung field to inferior 2/3 with crackles above, on right crackles to inferior 1/2 of lung fields posteriorly. Dullness to percussion of inferior left lung field posteriorly.
Abdomen:	Soft, non-tender, non-distended, no hepatosplenomegaly, no appreciable fluid wave.
Ext:	Bilateral lower extremities with 2+ pitting edema to knees, some hyperpigmentation to right lower extremity.

Labs/Studies:

CBC: 11.2/10.2/32.7/179
BMP: 141/3.9/103/30/15/0.85/107
INR: 0.9
BNP: 1857
UA: WBC 4, RBC 29 , +Bacteria, UCr 90, UPr 14
Rheum: CCP <16, ANCA neg, RF 936
Pleural Fluid: LDH 98 (serum 237), Protein 2.8 (serum 6.0), Glucose 107
Cytology: Reactive mesothelial cells, histiocytes, lymphocytes, signet cells

Imaging

CXR

There is a large left pleural effusion obscuring the lower half of the left hemi thorax. The cardiac silhouette is also obscured. There is pulmonary venous vascular congestion. There is also a right pleural effusion with fluid tracking into the minor fissure. Pulmonary interstitial edema is also noted.

CT Chest (High-Resolution):

Bilateral, left greater than right, pleural effusions with adjacent atelectasis and collapse versus consolidation of the left lower lobe.
Prominent main pulmonary artery measuring 3.3 cm in diameter, which can be seen with pulmonary arterial hypertension.

TTE:

LVEF is 50-55%.
Impaired left ventricular relaxation, which is associated with grade I/IV or mild diastolic dysfunction.
Moderate aortic stenosis with mild regurgitation (AVA 1.4 cm3, mean gradient 14mmHg, peak velocity 2.4 m/s).
Severe pulmonary hypertension (est PASP 52-62mmHg).
The inferior vena cava appeared dilated and decreased <50% with respiration (RAP 10-20 mmHg).
Minimal pericardial effusion without echocardiographic evidence of tamponade.

Assessment/Plan:

64F with history of CAD (prior MI), CHF, hypertension, CLL, hypothyroidism presented from a SNF with progressive shortness of breath, orthopnea and LE swelling, found to have bilateral (L>R) pleural effusion now s/p thoracentesis with transudative fluid.

#Acute hypoxic respiratory failure: Large pleural effusions, s/p thoracentesis with pleural fluid suggestive of transudative process. Most likely secondary to left ventricular diastolic dysfunction. Improved after thoracentesis and diuresis. High-resolution CT chest performed without evidence of autoimmune-related pulmonary fibrosis or ILD (though persistent pleural effusions, pulmonary vascular congestion).

#Pleural fluid signet cells: Identified on cytology, potentially related to history of untreated CLL or alternative primary malignancy.

#Left ventricular diastolic dysfunction, decompensated: Associated with pleural effusions and hypoxemic respiratory failure. Management with diuresis.

#Pulmonary Hypertension: Severe, noted on transthoracic echocardiography, may be secondary to hypoxemia associated with pleural effusions, consider repeat imaging once euvolemic or right-heart catheterization.

#Microscopic Hematuria: No evidence of infection, no symptoms suggestive of nephrolithiasis. No casts identified or significant proteinuria. Plan for renal ultrasound.

#Rheumatoid Arthritis: History of rheumatoid arthritis, on prednisone and hydroxychloroquine. Imaging without evidence of inflammatory arthropathy, RF elevated but CCP negative. Per rheumatology, the patient’s symptoms are not consistent with RA, continuing home medications while evaluation is ongoing. Pleural effusions unlikely associated with RA as transudative, and without monocyte predominance or low glucose.

Case 2: Malignant Pleural Effusion

Within the lungs there are ground-glass opacities bilaterally, and a left pleural effusion with adjacent consolidation vs compressive atelectasis.

Protein: 2.6 (serum: 4.9)
LDH: 1275 (serum: 219)
Cytology: Malignant cells

Case 3: Traumatic Thoracentesis

Moderate right pleural effusion, some fluid in non-dependent portions suggestive of loculation. Diffuse nodules and opacification in right lung with compressive atelectasis. Left pleural effusion with high density material at the posterior costophrenic angle. Left chest tube.

Protein: 2.7 (serum 6.4)
LDH: 344 (serum 236)
Cell count: 100,000 RBC

Case 4: Pneumonia

Loculated right pleural effusion with foci of atelectasis and consolidative changes concerning for pneumonia. Minimal left-sided pleural effusion with consolidative changes. Enlarged mediastinal lymph nodes, possibly reactive.

Protein: 4.3 (serum 6.7)
LDH: 377 (serum 108)
pH: 7.46
Glucose: 153
Neutrophils: 84%

Etiology of Pleural Effusions: ¹

Etiology	Frequency (%)
CHF	35
Pneumonia	22
Malignancy	15
Pulmonary Embolism	11

Clinical Features in the Diagnosis of Pleural Effusions and Identifying Etiology: ^1,2

Pleural effusions can be easily identified on chest radiography, physical examination findings include dullness to percussion, decreased tactile fremitus and decreased (or absent) breath sounds.

Hemoptysis: Malignancy, PE, TB
Weight Loss: Malignancy, TB
Ascites: Cirrhosis, ovarian cancer
Unilateral Leg Swelling: PE
Bilateral Leg Swelling: CHF, cirrhosis, nephrotic syndrome
Jugular Venous Distension: CHF

Differential Diagnosis of Pleural Effusions: ^1,2,3,4

References:

Light, R. W. (2002). Clinical practice. Pleural effusion. The New England journal of medicine, 346(25), 1971–1977. doi:10.1056/NEJMcp010731
McGrath, E. E., & Anderson, P. B. (2011). Diagnosis of pleural effusion: a systematic approach. American journal of critical care : an official publication, American Association of Critical-Care Nurses, 20(2), 119–27– quiz 128. doi:10.4037/ajcc2011685
Thomsen, T. W., DeLaPena, J., & Setnik, G. S. (2006). Videos in clinical medicine. Thoracentesis. The New England journal of medicine (Vol. 355, p. e16). doi:10.1056/NEJMvcm053812
Wilcox, M. E., Chong, C. A. K. Y., Stanbrook, M. B., Tricco, A. C., Wong, C., & Straus, S. E. (2014). Does this patient have an exudative pleural effusion? The Rational Clinical Examination systematic review. JAMA : the journal of the American Medical Association, 311(23), 2422–2431. doi:10.1001/jama.2014.5552
WikEM: Pleural effusion

Pulmonary Embolism in Hospitalized Patients

Brief Progress Note

Notified by nursing of abnormal vital signs, SpO2 91%. Briefly, this patient is a 52 year-old G1P1 with no prior medical history who is post-operative day three status post total abdominal hysterectomy, bilateral salpingoophorectomy as well as tumor debulking and staging for suspected primary ovarian adenocarcinoma based on peritoneal fluid cyctology.

On evaluation, the patient denied shortness of breath, chest pain, pleuritic chest pain, cough/hemoptysis, or calf/thigh pain. She states that she had been ambulating around the ward prior to having her vital signs assessed.

Physical Exam:

VS:	T	98.9	HR	94	RR	18	BP	117/72	O2	91% RA
Gen:	No acute distress, speaking in full sentences.
HEENT:	No jugular venous distension.
CV:	RRR, normal S1/S2, no prominent P2, no additional heart sounds.
Lungs:	Decreased breath sounds at inferior 1/3 posterior lung fields bilaterally, faint crackles above, no wheezing. Dullness to percussion in inferior lung fields.
Ext:	Warm, well-perfused. Sequential compression devices on bilateral lower extremities, removed revealing trace pitting edema symmetric bilaterally, no tenderness to palpation of posterior leg, no pain with passive dorsiflexion.

Medications:

Lovenox 40mg s.q. daily
Norco 5-325mg p.o. q.4.h. p.r.n. pain
Morphine 2mg i.v. q.3.h. p.r.n. breakthrough pain
Colace 100mg p.o. b.i.d. p.r.n. constipation
Zofran 4mg i.v. q.6.h. p.r.n. nausea/vomiting

Imaging:

CXR

Bilateral pleural effusions with pleural fluid tracking along the minor fissure.

CT Chest

No evidence of pulmonary embolism, study performed 5 days prior to onset of symptoms.

CT Abdomen/Pelvis

Significant peritoneal carcinomatosis, ascites delineates peritoneal from retroperitoneal spaces.

Assessment and Plan:

52yo G1P1 with likely primary ovarian adenocarcinoma with extensive peritoneal involvement, complicated by malignant ascites and pleural effusions with hypoxemia. The primary concern in this post-operative patient with a history of malignancy is venous thromboembolism, particularly pulmonary embolism. Aside from hypoxemia, this patient had no symptoms suggestive of pulmonary embolism (denied dyspnea, chest pain, cough, or lower extremity pain). Her examination had some signs infrequently associated with pulmonary embolism which were otherwise adequately explained by known bilateral pleural effusions (including decreased breath sounds, rales, and tachypnea), she was not tachycardic, had no evidence of jugular venous distension, nor a prominent P2. In addition, she was receiving appropriate VTE prophylaxis (both pharmacological and mechanical). The application of the Modified Wells clinical decision rule suggests low likelihood of pulmonary embolism (with 2.5 points assigned for recent surgery and history of malignancy). The patient had a recent CT chest without evidence of pulmonary embolism, and given that an elevated D-dimer was virtually assured which would have necessitated repeat imaging (and the associated risks of radiation exposure and contrast injury), the episode was ascribed to ventilation/perfusion mismatch secondary to large pleural effusions. Hypoxemia resolved after several minutes at rest and no further testing was performed.

Signs and Symptoms of Pulmonary Embolism¹

Signs	Symptoms
Tachypnea	Dyspnea (rest/exertion)
Tachycardia	Pleurtic chest pain
Rales	Cough
Decreased breath sounds	Orthopnea
Prominent P2	Calf/thigh pain or swelling
JVD	Wheezing

Modified Wells Criteria^1,2

Feature	Points
Clinical symptoms of DVT (leg swelling, tenderness to palpation)	3.0
Pulmonary embolism most likely diagnosis	3.0
Tachycardia (HR >100)	1.5
Immobilization >3d, surgery in prior 4 weeks	1.5
Prior DVT/PE	1.5
Hemoptysis	1.0
Malignancy	1.0

>4.0 Likely
≤4.0 Unlikely

Algorithm for Evaluation of Suspected Pulmonary Embolism²

Utility of D-Dimer:²: Of limited utility in patients with high suspicion for pulmonary embolism; Decreased specificity: malignancy, hospitalized patients, pregnancy, elderly
Efficacy of DVT prophylaxis:³: LMWH prevents approximately ½ of VTE events (including PE, symptomatic and asymptomatic DVT)

References:

Kruip, M. J. H. A., Söhne, M., Nijkeuter, M., Kwakkel-Van Erp, H. M., Tick, L. W., Halkes, S. J. M., Prins, M. H., et al. (2006). A simple diagnostic strategy in hospitalized patients with clinically suspected pulmonary embolism. Journal of internal medicine, 260(5), 459–466. doi:10.1111/j.1365-2796.2006.01709.x
Tapson, V. F. (2008). Acute pulmonary embolism. The New England journal of medicine, 358(10), 1037–1052. doi:10.1056/NEJMra072753
Själander, A., Jansson, J.-H., Bergqvist, D., Eriksson, H., Carlberg, B., & Svensson, P. (2008). Efficacy and safety of anticoagulant prophylaxis to prevent venous thromboembolism in acutely ill medical inpatients: a meta-analysis. Journal of internal medicine, 263(1), 52–60. doi:10.1111/j.1365-2796.2007.01878.x

Fever in Systemic Lupus Erythematosus

HPI:

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

PMH:

SLE
AVN left hip

PSH:

Total hip arthroplasty

FH:

Non-contributory

SHx:

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

Meds:

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

Allergies:

NKDA

Physical Exam:

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

Labs/Studies:

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

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

Imaging:

CXR: Negative for acute cardiopulmonary process.

Assessment/Plan:

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

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

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

Hospital Course:

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

Differential Diagnosis of Hypocalcemia: ^1,2

Laboratory Evaluation of Hypocalcemia: ^1,2

Clinical Manifestations of Hypocalcemia: ¹

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

Management of Symptomatic Hypocalcemia: ¹

10mL 10% Calcium Gluconate
Dilute in 100mL D5W

Fever in SLE:

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

Risk Factors for Infection:³

Neutropenia/Lymphopenia
Hypocomplementemia
Immunosuppressive therapy (especially Azathioprine⁴)

Laboratory Studies:³

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

References:

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

Electrolyte Abnormalities

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

Differential Diagnosis and Evaluation of Hyponatremia

Differential Diagnosis and Evaluation of Hypernatremia

Differential Diagnosis and Evaluation of Hypokalemia

Differential Diagnosis of Hyperkalemia

Differential Diagnosis of Hypo and Hypercalcemia

Differential Diagnosis of Hypo and Hypermagnesemia

Differential Diagnosis of Hypo and Hyperphosphatemia

References:

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

Biliary Duct Dilation

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

Ultrasound

CT Abdomen/Pelvis

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

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

References:

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

Acute Kidney Injury

Hospital Course:

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

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

Laboratory Studies

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

Urine electrolytes:

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

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

Imaging:

CT Abdomen/Pelvis with IV contrast

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

Assessment:

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

Definition of Acute Kidney Injury: ¹

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

Staging of Acute Kidney Injury: ¹

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

Management of Contrast-induced AKI: ²

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

Differential Diagnosis of Acute Kidney Injury: ³

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

Evaluation of AKI: ⁴

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

References:

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

Lower Extremity Edema

HPI:

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

PMH:

HTN
DM
Chronic EtOH abuse

PSH:

None

FH:

Unknown

SHx:

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

Meds:

None

Allergies:

NKDA

Physical Exam:

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

Labs/Studies:

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

Imaging:

Venous Lower Extremity Ultrasound

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

Assessment/Plan:

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

Mechanisms of Lower Extremity Edema: ¹

Differential Diagnosis of Lower Extremity Edema: ^1,2

Evaluation:

History ^1,2

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

Physical Exam ^1,2

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

Key Features Distinguishing Cellulitis: ³

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

References:

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

Lymphadenopathy Applied: Lymphoma

HPI:

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

Physical Exam:

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

Imaging:

CT Chest - Axial

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

CT Chest - Sagittal

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

Assessment/Plan:

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

Lymphadenopathy Applied – Lymphoma

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

Necrotizing Soft-Tissue Infection (NSTI)

HPI:

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

PMH:

Diabetes mellitus, diagnosed 8yrs ago

PSH:

None

FH:

Non-contributory

SHx:

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

Meds:

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

Allergies:

NKDA

Physical Exam:

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

Labs/Studies:

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

Imaging:

CT Lower Extremity

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

Assessment/Plan:

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

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

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

Skin and soft-tissue layers and their infections: ¹

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

Risk Factors

IVDA
Comorbid conditions
- DM
- Obesity
- Immunosuppression

Physical Exam

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

Treatment

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

LRINEC score ⁵

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

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

References:

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

Acute Respiratory Distress Syndrome

HPI:

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

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

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

PMH:

Mild asthma, not requiring medication
MRSA skin abscess

PSH:

None

FH:

Non-contributory.

SHx:

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

Meds:

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

Allergies:

NKDA

Physical Exam:

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

Labs/Studies:

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

Imaging

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

Assessment/Plan:

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

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

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

Pathophysiology of Acute Respiratory Distress Syndrome (ARDS):¹

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

Definition of ARDS (Berlin):^2,3

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

Causes of ARDS:^2,4

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

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

Breath Sequences:

Continuous Mandatory Ventilation (CMV)

All breaths controlled by ventilator, no triggered breaths.

Assist-Control Ventilation (AC)

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

Synchronized Intermittent Mandatory Ventilation (SIMV)

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

Pressure Support (PS)

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

Continuous Positive Airway Pressure (CPAP)

Spontaneous breathing at elevated baseline pressure.

Control Variables:

Volume Control (VC)

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

Pressure Control (PC)

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

Pressure-Regulated Volume Control (PRVC)

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

References:

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

Cervical Lymphadenopathy

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

Imaging:

Cervical Lymphadenopathy - Axial

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

Cervical Lymphadenopathy - Coronal

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

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

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

Lymph nodes and their drainage: ^1,2

Evaluation of Lymphadenopathy: ^2,3,4

References:

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

Hepatic Abscess

HPI:

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

Imaging:

Hepatic Abscess - Axial

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

Hepatic Abscess - Coronal

Assessment & Plan:

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

Differential Diagnosis of Hepatic Abscess:¹

References:

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

Alcoholic Hepatitis

HPI:

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

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

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

PMH:

EtOH abuse
Alcoholic hepatitis

PSH:

None

FH:

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

SHx:

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

Meds:

None

Allergies:

NKDA

Physical Exam:

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

Labs/Studies:

1mo prior to admission:

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

Day 1:

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

Day 4:

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

Imaging:

Abdominal US

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

Assessment/Plan:

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

Hospital Course

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

Pathophysiology of Alcoholic Hepatitis: ¹

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

Evaluation of Alcoholic Hepatitis: ^1,2

Clinical features:

Rapid onset jaundice
Tender hepatomegaly
Fever
Ascites
Proximal muscle loss
Encephalopathy

Labs:

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

Other studies:

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

Management of Alcoholic Hepatitis: ^1,2

Grading Severity:

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

Treatment:

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

Interpretation of Liver Function Tests: ³

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

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

References:

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

Joint Pain and Tremor

HPI:

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

PMH:

Arthritis
Gout

PSH:

Left tib/fib fracture s/p ORIF

FH:

No family history of RA, SLE or joint disease.

SHx:

No t/e/d use
Lives at home alone

Meds:

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

Allergies:

NKDA

Physical Exam:

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

Labs/Studies:

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

Assessment/Plan:

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

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

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

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

Differential Diagnosis of Monoarticular Arthralgia: ^1,2

Differential Diagnosis of Polyarticular Arthralgia ^1,3

Use of Serum Uric Acid in Acute Gout ⁴

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

Approach to Joint Pain: ³

Approach to Joint Pain

Certain key historical elements can help narrow the differential diagnosis.

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

Differential Diagnosis of Tremor: ^5,6

References:

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

Hyperglycemic Crises

CC:

Blurred vision, numbness

HPI:

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

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

PMH:

DM II
HTN

PSH:

None

FH:

Several maternal family members with DM.

SHx:

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

Meds:

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

Allergies:

NKDA

Physical Exam:

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

Labs/Studies:

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

Assessment/Plan:

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

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

Key signs/symptoms of HHS/DKA:

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

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

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

References:

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

Causes of Fever

Key Features

Immediate Evaluation and Management

Pathophysiology of Fever

References

Grid and Leads

Axis

Atrial Enlargement

Ventricular Hypertrophy

Secondary Repolarization Abnormalities

Bundle Branch Blocks

Left Bundle Branch Block

Right Bundle Branch Block

Hemiblocks

Other Blocks

Ischemia and Infarction

Coronary Artery Territories

External Links

HPI

Images

CT Chest: Lung Window

CT Body: Bone Window

Algorithm for the Evaluation of Anemia 1,2

References:

HPI:

Images

CT head without contrast one hour after presentation

CT head without contrast on hospital day 5

Algorithm for the Management of Severe Traumatic Brain Injury1,2

References

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs/Studies:

Imaging:

Assessment/Plan:

Differential Diagnosis of Elevated Serum Lactate 1,2

Algorithm for Evaluation of Acidemia 3,4

Algorithm for Evaluation of Alkalemia 3,4

References:

HPI:

Hospital Course:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs/Studies:

Imaging

Assessment/Plan:

Case 2: Malignant Pleural Effusion

Case 3: Traumatic Thoracentesis

Case 4: Pneumonia

Etiology of Pleural Effusions: 1

Clinical Features in the Diagnosis of Pleural Effusions and Identifying Etiology: 1,2

Differential Diagnosis of Pleural Effusions: 1,2,3,4

References:

Brief Progress Note

Physical Exam:

Medications:

Imaging:

CXR

CT Chest

CT Abdomen/Pelvis

Assessment and Plan:

Signs and Symptoms of Pulmonary Embolism1

Modified Wells Criteria1,2

Algorithm for Evaluation of Suspected Pulmonary Embolism2

References:

HPI:

PMH:

PSH:

FH:

Algorithm for the Evaluation of Anemia ^1,2

Algorithm for the Management of Severe Traumatic Brain Injury^1,2

Differential Diagnosis of Elevated Serum Lactate ^1,2

Algorithm for Evaluation of Acidemia ^3,4

Algorithm for Evaluation of Alkalemia ^3,4

Etiology of Pleural Effusions: ¹

Clinical Features in the Diagnosis of Pleural Effusions and Identifying Etiology: ^1,2

Differential Diagnosis of Pleural Effusions: ^1,2,3,4

Signs and Symptoms of Pulmonary Embolism¹

Modified Wells Criteria^1,2

Algorithm for Evaluation of Suspected Pulmonary Embolism²

Differential Diagnosis of Hypocalcemia: ^1,2

Laboratory Evaluation of Hypocalcemia: ^1,2

Clinical Manifestations of Hypocalcemia: ¹

Management of Symptomatic Hypocalcemia: ¹

Risk Factors for Infection:³

Laboratory Studies:³

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

Definition of Acute Kidney Injury: ¹

Staging of Acute Kidney Injury: ¹

Management of Contrast-induced AKI: ²

Differential Diagnosis of Acute Kidney Injury: ³

Evaluation of AKI: ⁴

Mechanisms of Lower Extremity Edema: ¹

Differential Diagnosis of Lower Extremity Edema: ^1,2

History ^1,2

Physical Exam ^1,2