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Critical Care

Last 50 Critical Care Postings

(Click on title to be directed to posting, most recent listed first, CME offerings in Bold)

Severe Accidental Hypothermia in Phoenix? Active Rewarming Using 
   Thoracic Lavage
Left Ventricular Assist Devices: A Brief Overview
July 2019 Critical Care Case of The Month: An 18-Year-Old with
   Presumed Sepsis and Progressive Multisystem Organ Failure 
An Observational Study Demonstrating the Efficacy of Interleukin-1 
   Antagonist (Anakinra) in Critically-ill Patients with Hemophagocytic
Which Half Are You? Almost Half of Pediatric Oncologists and Intensivists
   Are Burnt Out……
Management of Refractory Hypoxemic Respiratory Failure Secondary to
   Diffuse Alveolar Hemorrhage with Venovenous Extracorporeal Membrane
Amniotic Fluid Embolism: A Case Study and Literature Review
April 2019 Critical Care Case of the Month: A Severe Drinking
Ultrasound for Critical Care Physicians: An Unexpected Target Lesion
January 2019 Critical Care Case of the Month: A 32-Year-Old Woman
   with Cardiac Arrest
The Explained Variance and Discriminant Accuracy of APACHE IVa 
Severity Scoring in Specific Subgroups of ICU Patients
Ultrasound for Critical Care Physicians: Characteristic Findings in a 
   Complicated Effusion
October 2018 Critical Care Case of the Month: A Pain in the Neck
Ultrasound for Critical Care Physicians: Who Stole My Patient’s Trachea?
August 2018 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Caught in the Act
July 2018 Critical Care Case of the Month
June 2018 Critical Care Case of the Month
Fatal Consequences of Synergistic Anticoagulation
May 2018 Critical Care Case of the Month
Airway Registry and Training Curriculum Improve Intubation Outcomes in 
   the Intensive Care Unit
April 2018 Critical Care Case of the Month
Increased Incidence of Eosinophilia in Severe H1N1 Pneumonia during 2015
   Influenza Season
March 2018 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Ghost in the Machine
February 2018 Critical Care Case of the Month
January 2018 Critical Care Case of the Month
December 2017 Critical Care Case of the Month
November 2017 Critical Care Case of the Month
A New Interventional Bronchoscopy Technique for the Treatment of
   Bronchopleural Fistula
ACE Inhibitor Related Angioedema: A Case Report and Brief Review
Tumor Lysis Syndrome from a Solitary Nonseminomatous Germ Cell Tumor
October 2017 Critical Care Case of the Month
September 2017 Critical Care Case of the Month
August 2017 Critical Care Case of the Month
Telemedicine Using Stationary Hard-Wire Audiovisual Equipment or Robotic 
   Systems in Critical Care: A Brief Review
Carotid Cavernous Fistula: A Case Study and Review
July 2017 Critical Care Case of the Month
High-Sensitivity Troponin I and the Risk of Flow Limiting Coronary Artery 
   Disease in Non-ST Elevation Acute Coronary Syndrome (NSTE-ACS)
June 2017 Critical Care Case of the Month
Clinical Performance of an Interactive Clinical Decision Support System for 
   Assessment of Plasma Lactate in Hospitalized Patients with Organ
May 2017 Critical Care Case of the Month
Management of Life Threatening Post-Partum Hemorrhage with HBOC-201 
   in a Jehovah’s Witness
Tracheal Stoma Necrosis: A Case Report
April 2017 Critical Care Case of the Month
March 2017 Critical Care Case of the Month
Ultrasound for Critical Care Physicians: Unchain My Heart
February 2017 Critical Care Case of the Month
January 2017 Critical Care Case of the Month
December 2016 Critical Care Case of the Month


For complete critical care listings click here.

The Southwest Journal of Pulmonary and Critical Care publishes articles directed to those who treat patients in the ICU, CCU and SICU including chest physicians, surgeons, pediatricians, pharmacists/pharmacologists, anesthesiologists, critical care nurses, and other healthcare professionals. Manuscripts may be either basic or clinical original investigations or review articles. Potential authors of review articles are encouraged to contact the editors before submission, however, unsolicited review articles will be considered.



Refractory Cardiogenic Shock

Bhupinder Natt, MD (

Tauseef Afaq Siddiqi, MD (

Jarrod Mosier, MD (

Yuval Raz, MD (

Department of Medicine, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, University of Arizona, Tucson, AZ



We present a case of refractory cardiogenic shock secondary to myxedema crises that was treated successfully with thyroid hormone replacement.

Case Presentation

History of Present Illness

A 62-year-old woman with past medical history significant only for hypothyroidism was seen in the emergency department (ED) after a fall at home. On further evaluation, the patient’s husband reported history consistent with deteriorating mental function as evident by speech alteration, inability to operate home appliances like the coffeemaker and gradually worsening generalized weakness. She was recently seen at an outside hospital the week previous to this admission and given a prescription for furosemide for pedal edema.

ED evaluation showed her to be lethargic, disoriented with progressively deteriorating mentation, with hypothermia and bradycardia. Her progressive decline in mentation led to endotracheal intubation for airway protection. The patient was started on vasopressors due to post-intubation hypotension and transferred to the Medical Intensive Care Unit (MICU).

Vitals and Physical Exam

Vitals upon presentation to ED: Temperature 29o Celsius; Heart Rate 42 bpm; Blood Pressuren107/79 mm Hg; Respiratory Rate 14/min; SpO2 97 % on Room Air.

Vitals upon arrival in MICU: Temperature of 29o Celsius; Heart Rate 43 bpm; Blood Pressure 111/57 mmHg; Respiratory Rate of 10/min; SpO2 100% on mechanical ventilation;

Neurologically, she was sedated with no obvious localizing signs. Skin exam revealed a sutured scalp lesion and scattered abrasion on arms. Cardiopulmonary exam was significant only for bradycardia, which was determined to be sinus rhythm by the electrocardiogram (EKG). Other system examination was significant only for 2+ non-pitting edema of upper and lower extremities.

Laboratory and Radiology Data

CBC: White Cell Count 8.4x1000/microL; Hemoglobin 9.5 g/dL; MCV 100 fL; Platelets 82x1000/microL.

Electrolytes and Metabolic Panel: Sodium 134 mMol/L; Potassium 4.2 mMol/L; Chloride 97 mMol/L; Bicarbonate 26 mMol/L; Urea Nitrogen 38 mg/dL; Creatinine 0.9 mg/dL. Glucose 78 mg/dL; Calcium 9.6 mg/dL.

Total Protein 6.3 g/dL; Albumin 3.7 g/dL; Bilirubin 0.7 mg/dL; Alkaline Phosphate 104 IU/L; ALT 72 IU/L; AST 158 IU/L; TSH 36.1 uIU/mL; Thyroxine 0.8 ng/dL; Free T3 1.2 pg/mL (Normal 2.4-4.2 pg/mL); Cortisol 20.3 mcg/dL.

ABG: pH 7.52; PaCO2 34; PaO2 166; HCO3 28; SaO2 97.6 % on 50% FiO2.

Urine Analysis: Negative.

Urine Drug Screen: Negative.

Chest X-Ray: Emphysematous changes with no acute cardiopulmonary process.

Non-contrast CT of the head and cervical spine: Unremarkable except scalp hematoma.

EKG at Presentation

MICU Course

After initial stabilization of blood pressure in ED; receiving four liters of intravenous fluids; and norepinephrine infusion at increasing doses, she was transferred to MICU. She required two more liters of crystalloids, vasopressin and increasing doses of norepinephrine, epinephrine, phenylephrine and dobutamine infusions. Corticosteroid was added for refractory shock. She also received first dose of broad-spectrum antimicrobials in ED.

Two hours after arrival to the MICU, seven hours post presentation to the ED; a Swan-Ganz pulmonary artery catheter was placed. The values obtained from the Swan-Ganz catheter are reported in table 1. 

These values were obtained seven hours into admission, while the patient was being actively rewarmed, treated with a total of six liters (L) of crystalloid solutions and on norepinephrine at 13 mcg/min and dobutamine at 5 mcg/kg/min.

The patient remained hypotensive and sequentially, within hours, multiple vasopressors and inotropic agents were required. Table 2 reports the vitals and values off the Swan-Ganz catheter 12 hours after initial placement, when the patient is being actively rewarmed, treated for close to 18 hours and while receiving intravenous epinephrine at 3 mcg/min, norepinephrine at 30 mcg/min, vasopressin a 0.03 units/min, phenylephrine at 150 mcg/min and dobutamine at 20 mcg/min. 

A formal 2-D echocardiogram was obtained which showed a global left ventricular dysfunction and hypokinesis with reduced ejection fraction of 35% and mildly reduced right ventricular dysfunction. No major valvular or pericardial pathology was noticed. Given the patient’s history and clinical features of hypothyroidism, a diagnosis of myxedema coma was made and treatment started with levothyroxine 125 mcg a day intravenously. Corticosteroids were discontinued due to concern of blockage of peripheral conversion of T4 to T3. T3 was unavailable in our city initially but was subsequently obtained and prescribed to our patient at 25 mcg of liothyronine three times a day. She responded very well to the treatment and was successfully weaned off all vasopressor support, liberated from mechanical ventilation on the fourth day and transferred out of the MICU on day five of admission. Limited repeat echocardiogram prior to transfer out of the MICU showed an ejection fraction of 65%.

Cultures, lumbar puncture and all imaging including brain MRI obtained during admission and MICU stay remained negative. A potential precipitating factor was not found and all empiric treatments were gradually withdrawn prior to the transfer out of MICU.

Retrospective history taking revealed patients’ non-compliance with levothyroxine treatment for the past 2 years. She had been given a dose of levothyroxine while she was admitted at the outside hospital the week previously leading to her relatively normal T4 level, suggesting inhibited peripheral conversion to T3 and thus the limited effect of intravenous levothyroxine initially. Surprisingly, despite the ordeal, she continued to refuse to take the medication once extubated and transferred to Medicine.


A myxedema crisis is an extreme and life-threatening form of hypothyroidism that requires prompt diagnosis and treatment. Mortality rate has been reported as high as 60% despite appropriate diagnosis and management (1,2). Infections and discontinuation of thyroid supplements are the major precipitating factors. Other precipitants include hypothermia, gastrointestinal bleeding, congestive heart failure, cerebrovascular accident, metabolic disturbance and sedative drugs (3).

Myxedema crises manifests by involving multiple organ systems. Hypothermia can be profound and is usually the first sign of myxedema coma. Neuropsychiatric manifestations include confusion, lethargy, coma, psychosis (myxedema madness), and seizures. Respiratory depression is common likely due to depressed hypoxic and hypercapnic respiratory drive. Edema (myxedema) involving upper airways contributes to acute respiratory failure. Reduced intestinal motility leads to constipation, paralytic ileus and mega colon. Urine retention from bladder atony can be seen. Reduced glomerular filtration and reduced water excretion leads to hyponatremia, a consistent finding in myxedema crises.

Cardiovascular effects of myxedema crises include conduction abnormalities, reduced contractility, cardiomegaly and pericardial effusion. Sinus bradycardia, low voltage complexes, bundle branch blocks, complete heart blocks, and nonspecific ST-T changes in electrocardiogram have been reported. Prolonged QT interval and polymorphic ventricular tachycardia has been described as well (4). Depressed cardiac contractility leads to low stroke volume and cardiac output. Animal studies have documented that hypothyroidism leads to cardiomegaly from cardiac atrophy, impaired myocardial blood flow and loss of arterioles resulting in severe systolic dysfunction (5).

These cardiogenic effects of hypothyroid state leading to depressed ionotropy and chronotropy with compensatory vasoconstriction are believed to be a result of low intracellular T3. The hypothyroid heart attempts to perform by better coupling of ATP to contractile events until a precipitating event disrupts this fine balance (6). This resultant de-compensation leads to hypotension and cardiogenic shock that may not respond to vasopressors alone until thyroid hormone replacement is given.

Treatment usually involves intensive care admission with cardiopulmonary support, aggressive fluid and electrolyte management, treatment of underlying and precipitating factors and thyroid hormone replacement. Intravenous T4 is the most commonly used preparation as intestinal absorption may not be reliable. In severe illness, the conversion of T4 to T3 by 5’-monodeiodinase is impaired. Intravenous T3 preparation should be used. Improved cardiac function is reported in 24 hours when T3 replacement is used and it may take up to a week to notice beneficial effects with T4 replacement alone (7).


  1. Mathew V, Misgar RA, Ghosh S, Mukhopadhyay P, Roychowdhury P, Pandit K, Mukhopadhyay S, Chowdhury S. Myxedema Coma: a new look into an old crisis. J Thyroid Res. 2011:493462.[CrossRef] [PubMed]
  2. Wartofsky L, Myxedema Coma, Endocrinol Metab Clin N Am. 2006; 35(4): 687-98. [CrossRef][PubMed]
  3. Brent GA, Davies TF. Hypothyroidism and thyroiditis. In: Melmed S, Polonsky KS, Reed P, Kronenberg HM, eds. Williams Textbook of Endocrinology. Philadelphia, PA: WB Saunders, 2008.
  4. Schenck JB, Rizvi AA, Lin T. Severe primary hypothyroidism manifesting with torsades de pointes. Am J Med Sci. 2006 Mar; 331(3): 154-6. [CrossRef] [PubMed] 
  5. Tang YD, Kuzman JA, Said S, Anderson BE, Wang X, Gerdes AM. Low thyroid function leads to cardiac atrophy with chamber dilatation, impaired myocardial blood flow, loss of arterioles, and severe systolic dysfunction. Circulation. 2005;112(20):3122-30. [CrossRef] [PubMed]
  6. W. M. Wiersinga. Hypothyroidism and myxedema coma. In: Jameson JL, Legroot LJ, eds. Endocrinology: Adult and Pediatric. Philadelphia, PA: Saunders Elseiever, 6th edition, 2010:1607-22.
  7. MacKerrow SD, Osborn LA, Levy H, Eaton RP, Economou P. Myxedema associated cardiogenic shock treated with intravenous triiodothyronine. Ann Int Med. 1992;117:1014-5. [CrossRef][PubMed] 

Reference as: Natt B, Siddiqi TA, Mosier J, Raz Y. Refractory cardiogenic shock. Southwest J Pulm Crit Care. 2013;7(4):246-50. doi: PDF


Ultrasound for Critical Care Physicians: Right Diagnosis, Wrong Place

The patient was a 76 year old man, with a history of a prosthetic aortic valve (aortic stenosis) and chronic myelogenous leukemia.  He presented with fever and cough, and was found to have pneumonia with Klebsiella pneumonia cultured from a BAL. However, he also had persistent Enterococcus faecalis bacteremia and a new 3/6 diastolic murmur. 

An ultrasound of the heart was performed (Figures 1 and 2).

Figure 1. Parasternal long axis view of the heart.


Figure 2. Four chamber view of the heart.


Which of the following is the likely diagnosis?

  1. Aortic dissection
  2. Aortic valve endocarditis
  3. Displacement of the aortic valve
  4. Mitral valve endocarditis
  5. Tricuspid endocarditis

Reference as: Raschke RA. Ultrasound for critical care physicians: right diagnosis, wrong place. Southwest J Pulm Crit Care. 2013;7(4):232-5. doi: PDF



October 2013 Critical Care Case of the Month: Slow to Respond

Michael P. Mohning, MD


Pulmonary Sciences and Critical Care Medicine

University of Colorado Hospital

Denver, CO


History of Present Illness

A 66-year-old woman presents with confusion and lower extremity edema. She was brought to the emergency department by her family after 2-3 days of increasing confusion.  She has fatigue and a dry non-productive cough but denies shortness of breath, chest pain, fevers or chills. She had a decrease in oral intake and constipation for several days.


Five months ago, she was admitted to a hospital for community acquired pneumonia and hyponatremia. She is a never smoker, and doesn’t use alcohol.

There is no significant family history.


  • Omega 3 fatty acids
  • Multivitamins

Physical Examination

Temperature 36.1° C, blood pressure 106/61 mm Hg, heart rate 72 beats/min, respiratory rate 15 breaths/min, oxygen saturation 90% on room air.

She was confused, and oriented to self only.  She had facial edema.  Cardiac exam was normal. Pulmonary findings include rales at the lung bases. Her abdomen was non-tender, with active bowel sounds. She had 1+  lower extremity edema, no rashes, and delayed relaxation of reflexes.


She was anemic with hematocrit of 32%, hemoglobin 11 g/dL and WBC 5,000. Serum sodium is low at 118 meq/L, anion gap was normal at 9 and potassium and calcium levels were normal. Albumin is low at 3.2 g/dL. Remaining liver function, blood glucose and creatinine are normal. EKG shows no T wave inversions or ST segment elevation.


Chest x-ray is shown in figure 1.


Figure 1. Admission PA (Panel A) and lateral (Panel B) chest x-ray.

Which best describes the chest-x-ray?

  1. Bilateral interstitial infiltrates
  2. Enlarged cardiac silhouette
  3. Hyperexpanded lungs
  4. Poor inspiratory effort
  5. Pulmonary edema

Reference as: Mohning MP. October 2013 critical care case of the month: slow to respond. Southwest J Pulm Crit Care. 2013;7(4):214-20. doi: PDF


Ultrasound for Critical Care Physicians: Connecting Disparate Symptoms

An 18-year-old woman was recently diagnosed with non-ACTH-Mediated Cushing syndrome, now with a complaint of mild shortness of breath.

Her cardiac exam showed normal sinus rhythm at 84 beats per minute and blood pressure of 130/80 mmHg. Her mitral first heart sound was slightly accentuated, but the pulmonic sound was normal. Grade-I diastolic murmur was heard over the mitral area. Opening snap was absent. Lungs were clear and chest radiograph showed slight cardiomegaly. She had multiple freckles on his face and trunk and along the vermillion border of the lips.

An ultrasound of the heart was performed (Figure 1).

Figure 1. Four chamber view of the heart.


Which of the following is the likely diagnosis?

  1. Brugada syndrome
  2. Carney syndrome
  3. Gotway syndrome
  4. Jervell and Lange-Nielsen syndrome
  5. Peutz-Jeghers syndrome

Reference as: Gotway MB. Ultrasound for critical care physicians: connecting disparate symptoms. Southwest J Pulm Crit Care. 2013;7(3):176-8. doi: PDF


September 2013 Critical Care Case of the Month: Revenge of the Pharaohs

Robert A. Raschke, MD

Elijah Poulos, MD

Banner Good Samaritan Regional Medical Center

Phoenix, AZ


History of Present Illness

The patient was a 68 year-old man, admitted to our ICU through the emergency room (ER) in July 2013 with suspected urinary tract origin sepsis.

The patient was evaluated in ER by the ICU team. He was in his usual state of general good health until he visited his primary care physician for what he felt was a left inguinal hernia, and underwent a prostate examination, four days previously. The patient associated this prostate examination with the onset of fevers and chills that began the next morning. He was seen in an urgent care center where he was told his urinalysis was normal, and antibiotics were not prescribed. Over the intervening 3 days, he suffered recurrent fevers, had vomited three times, and had one diarrheal bowel movement. Earlier on the day of presentation, he had been mowing his lawn (in >100° F environment) and had become a little dizzy. His wife, a retired nurse, finally convinced him to report to the ER.

He denied dysuria, urinary frequency or urgency, headache, sore throat, cough, or abdominal pain.


He had a prior history of hypertension, gastroesophageal reflux, gout and hypercholesterolemia. He drank alcohol about twice a month and did not smoke.

There was no family history of illnesses.


  • Atorvastatin
  • Allopurinol
  • Hydrochlorothiazide
  • Lisinopril
  • Temazepam

Physical Exam

On ER triage, his temperature was 41.2° C, but vitals at the time of our initial examination were temp 38.2° C, HR 93 beats/min, BP 103/48 mm Hg, and respiratory rate 20 breaths/min. He was awake and alert, but made a few errors while relating his history – for instance, he initially answered yes when asked if he had a headache, then corrected himself and said no – he meant he had a fever. He was actively rigoring. HEENT exam was unrevealing. He had no lymphadenopathy. His lungs were clear. His abdomen was soft and nontender. He had a sliding left inguinal hernia that was not tender. None of his joints were acutely inflamed. His prostate was not enlarged or tender to palpation. He had no focal neurological deficits.


Pertinent laboratory values in the ER:

  • WBC: 7.7 x109/L
  • Hematocrit: 38.4%
  • Sodium: 131 me/L
  • Potassium: 3.1 me/L
  • BUN:28 g/dL
  • Creatinine: 1.3 mg/dL
  • Lactate: 2.1 mMol/L.

The rest of his admission labs and urinalysis were unremarkable.

Chest Radiography

His initial portable chest x-ray is shown in Figure 1.

Figure 1. Initial portable chest x-ray.


Which of the following is the likely cause of his fever?

  1. Prostatitis exacerbated by digital rectal exam
  2. Right middle lobe pneumonia
  3. Urinary tract infection
  4. All of the above
  5. None of the above

Reference as: Raschke RA, Poulos E. September 2013 critical care case of the month: revenge of the pharaohs. Southwest J Pulm Crit Care. 2013;7(3):142-50. doi: PDF