A 50 year-old male with a history of colonic mucinous adenocarcinoma on chemotherapy presented with a chief complaint of “vomiting”. He was unwilling to provide further history, repeating that he had vomited blood prior to presentation. His initial vital signs were notable for tachycardia. Physical examination showed some dried vomitus, brown in color, at the nares and lips; left upper quadrant abdominal tenderness to palpation; and guaiac-positive stool. Point-of-care hemoglobin was 3g/dL below the most recent measure two months prior. As his evaluation progressed, he developed hypotension and was transfused two units of uncrossmatched blood with adequate blood pressure response – he was started empirically on broad-spectrum antibiotics for an intra-abdominal source. Notable laboratory findings included a normal hemoglobin/hematocrit, acute kidney injury, and elevated anion gap metabolic acidosis presumably attributable to serum lactate of 10.7mmol/L. Computed tomography of the abdomen and pelvis demonstrated pneumoperitoneum with complex ascites concerning for bowel perforation. The patient deteriorated, was intubated, started on vasopressors and admitted to the surgical intensive care unit. The initial operative report noted extensive adhesions and perforated small bowel with feculent peritonitis. He has since undergone multiple further abdominal surgeries and remains critically ill.
Free air is seen diffusely in the non-dependent portions of the abdomen: in the anterior abdomen and pelvis, inferior to the diaphragm, and in the perisplenic region. There is complex free fluid in the abdomen.
Algorithm for the Evaluation of Hypotension1
This process for the evaluation of hypotension in the emergency department was developed by Dr. Ravi Morchi. In the case above, a systematic approach to the evaluation of hypotension using ultrasonography and appropriately detailed physical examination may have expedited the patient’s care. The expertly-designed algorithm traverses the cardiovascular system, halting at evaluable checkpoints that may contribute to hypotension.
- The process begins with the cardiac conduction system to identify malignant dysrhythmias (bradycardia, or non-sinus tachycardia >170bpm), which, in unstable patients are managed with electricity.
- The next step assesses intravascular volume with physical examination or bedside ultrasonography of the inferior vena cava. Decreased right atrial pressure (whether due to hypovolemia, hemorrhage, or a distributive process) is evidenced by a small and collapsible IVC. If hemorrhage is suspected, further ultrasonography with FAST and evaluation of the abdominal aorta may identify intra- or retroperitoneal bleeding.
- If a normal or elevated right atrial pressure is identified, evaluate for dissociation between the RAP and left ventricular end-diastolic volume. This is typically caused by a pre- or intra-pulmonary obstructive process such as tension pneumothorax, cardiac tamponade, massive pulmonary embolism, pulmonary hypertension, or elevated intra-thoracic pressures secondary to air-trapping. Thoracic ultrasonography can identify pneumothorax, pericardial effusion, or signs of elevated right ventricular systolic pressures (RV:LV, septal flattening).
- Assuming adequate intra-vascular volume is arriving at the left ventricle, rapid echocardiography can be used to provide a gross estimate of cardiac contractility and point to a cardiogenic process. If there is no obvious pump failure, auscultation may reveal murmurs that would suggest systolic output is refluxing to lower-resistance routes (ex. mitral insufficiency, aortic insufficiency, or ventricular septal defect).
- Finally, if the heart rate is suitable, volume deficits are not grossly at fault, no obstructive process is suspected, and cardiac contractility is adequate and directed appropriately through the vascular tree, the cause may be distributive. Physical examination may reveal dilated capillary beds and low systemic vascular resistance.
- Morchi R. Diagnosis Deconstructed: Solving Hypotension in 30 Seconds. Emergency Medicine News. 2015.
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.
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 Injury1,2
- 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
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
- 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
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.
- Mild asthma, not requiring medication
- MRSA skin abscess
- 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.
- 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
||PRVC, VT 320, RR 35, PEEP 6, FiO2 95%
||Young male, thin-appearing, intubated and sedated and not responding to verbal commands
||PERRL, unable to assess EOM, ET tube in place
||RRR, normal S1/S2, no murmurs
||Coarse breath sounds bilaterally
||Normoactive bowel sounds, soft, non-distended, no hepatosplenomegaly
||No clubbing, cyanosis, edema
||Unable to assess
- 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
Evidence of pneumomediastinum and pneumopericardium. Bilateral pulmonary infiltrates, but no pulmonary embolism.
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
||Acute in onset (<1 week)
|Origin of pulmonary edema
||Not explained by heart failure or fluid overload (assessed with echocardiography)
- 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.
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.
Volume Control (VC)
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 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-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)
- 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.
62M with a history of hepatitis C cirrhosis complicated by hepatocellular carcinoma s/p radiofrequency ablation presenting after referral from hepatology clinic for hyponatremia. One week ago, the patient developed abdominal distension and shortness of breath that resolved after large-volume paracentesis and was started on furosemide 40mg p.o. daily and aldactone 100mg p.o. daily.
After initiating diuretics, the patient noted worsening lower extremity edema, and increased thirst/fluid intake.
He reports two days of fatigue and intermittent confusion supported by family members who reported slowed speech. He otherwise denies abdominal pain, distension, nausea/vomiting, diarrhea/constipation, chest pain or shortness of breath. In the ED, the patient received 1L NS bolus.
- Hepatitis C cirrhosis c/b HCC s/p RFA
- Rheumatoid arthritis, well-controlled without medications
- Lives with partner, denies current or prior t/e/d abuse
- HepC contracted from blood transfusions
- Furosemide 40mg p.o. daily
- Spironolactone 100mg p.o. daily
- Rifaximin 550mg p.o. b.i.d.
||PRVC, VT 320, RR 35, PEEP 6, FiO2 95%
||Elderly female in no acute distress, alert and answering questions appropriately.
||NC/AT, PERRL, EOMI, no scleral icterus, MMM.
||RRR, normal S1/S2, no murmurs. JVP 8cm.
||Faint basilar crackles on bilateral lung bases.
||Normoactive bowel sounds, non-distended, non-tender, without rebound/guarding.
||2+ pitting edema in lower extremities to knees bilaterally. 2+ peripheral pulses, warm and well perfused.
||AAOx3. CN II-XII intact. No asterixis. Normal gait. Normal FTN/RAM.
- BMP (admission): 112/5.6/88/22/28/1.1/97
- BMP (+10h): 118/5.4/93/23/26/1.0/133
- sOsm: 264
- Urine: Na <20, K 26, Osm 453
- BNP: 40
- AST/ALT/AP/TB/Alb: 74/57/91/2.4/2.2
62M hx HepC cirrhosis, newly decompensated with e/o decompensation (new-onset ascites) and hyponatremia.
# hyponatremia: Sodium 114, likely chronic, patient currently asymptomatic without concerning findings on neurological exam. Clinical findings suggestive of hypervolemic hyponatremia 2/2 decompensated cirrhosis resulting in decreased effective arterial blood volume and volume retention. However, the recent initiation of diuretics, mild AKI and early response to isotonic fluids in the ED suggests possible hypovolemic component.
- 1L fluid restriction
- q.4.h. sodium check, goal increase of 8mEq per 24h
- hold diuretics
# hyperkalemia: Potassium 5.6, asymptomatic, AKI vs. medication-induced (aldactone). Continue monitoring.
# AKI: Elevated creatinine 1.1 from baseline 0.7. Likely pre-renal given recent initiation of diuretics. Consider hepatorenal syndrome given decompensated cirrhosis. Follow-up repeat creatinine after 1L NS bolus in ED.
# hepatitis C: decompensated with new-onset ascites. No e/o encephalopathy, continue home rifaximin.
Physiology of Hyponatremia: 1,2,3,4
Differential Diagnosis of Hyponatremia: 5
Evaluation of Hyponatremia: 2
- Identification of onset (acute vs. chronic)
- Presence of symptoms (HA, nausea, confusion, seizures)
- Assessment of volume status (edema, JVD, skin turgor, postural BP)
- Medical history (cardiac, liver, renal disease), drug history
- Freda BJ, Davidson MB, Hall PM. Evaluation of hyponatremia: a little physiology goes a long way. Cleve Clin J Med. 2004;71(8):639–650.
- Biswas M, Davies JS. Hyponatraemia in clinical practice. Postgrad Med J. 2007;83(980):373–378. doi:10.1136/pgmj.2006.056515.
- Adrogué HJ, Madias NE. Hyponatremia. N. Engl. J. Med. 2000;342(21):1581–1589. doi:10.1056/NEJM200005253422107.
- Marx JA, Hockberger RS, Walls RM, Adams JG. Rosen’s emergency medicine: concepts and clinical practice. 2010;1.
- Milionis HJ, Liamis GL, Elisaf MS. The hyponatremic patient: a systematic approach to laboratory diagnosis. CMAJ. 2002;166(8):1056–1062.