Ultrasound for Critical Care Physicians: The Pleura and the Answers that Lie Within

Heidi L. Erickson MD 

Division of Pulmonary, Critical Care and Occupational Medicine

University of Iowa Hospitals and Clinics

Iowa City, IA

A 67-year-old woman with a 40-pack-year smoking history was admitted to the intensive care unit with acute respiratory failure secondary to adult respiratory distress syndrome (ARDS) in the setting of pneumococcal bacteremia. On admission, she required endotracheal intubation and vasopressor support.  She was ventilated using a low tidal volume strategy and was relatively easy to oxygenate with a PEEP of 5 and 40% FiO2. After 48 hours of clinical improvement, the patient developed sudden onset tachypnea and increased peak and plateau airway pressures. A bedside ultrasound was subsequently performed (Figures 1 and 2).

Figure 1. Two- dimensional ultrasound image of the right lung with associated M-mode image.

Figure 2. Two- dimensional ultrasound image of the left lung with associated M-mode image.

What is the cause of this patient’s acute respiratory decompensation and increased airway pressures? (Click on the correct answer for an explanation)

1. Pericardial effusion
2. Pneumothorax
3. Pulmonary edema
4. Pulmonary embolism

Cite as: Erickson HL. Ultrasound for critical care physicians: the pleura and the answers that lie within. Southwest J Pulm Crit Care. 2015;11(6):260-3. doi: http://dx.doi.org/10.13175/swjpcc149-15 PDF

December 2015 Critical Care Case of the Month

Samir Sultan, DO 

Banner University Medical Center Phoenix

Phoenix, AZ 

History of Present Illness

The patient is a 32-year-old woman who presented with flank pain for 3 days to an outside hospital. She was diagnosed with pyelonephritis and begun on ceftriaxone. She was discharged against medical advice on cephalexin.

She returned to the same hospital 3 days later by ambulance with labored breathing and weakness and was emergently intubated. She was transferred for ventilator management and respiratory failure.

Past Medical History

She has a long history of poorly controlled diabetes mellitus.

Physical Examination

She is orally intubated and sedated.

Vitals: Temperature - 100.9º F, Blood Pressure - 117/75 mm Hg, Heart Rate - 148 beats per minute,  Respiratory Rate - 31 breaths/min, SpO2 - 88 % on assist control of 30, tidal volume of 350 mL, PEEP 15, and an FiO2 100%.

There is scatted rhonchi and rales but the remainder of the physical examination is unremarkable.

Radiography

Her admission portable chest X-ray is shown in Figure 1.

Figure 1. Admission portable AP of the chest.

Which of the following should be ordered as part of her initial work-up? (Click on the correct answer to proceed to the second of five panels).

1. Administer broad spectrum antibiotics
2. Blood and urine cultures
3. Rapid influenza test
4. 1 and 3
5. All of the above

Cite as: Sultan S. December critical care case of the month. Southwest J Pulm Crit Care. 2015;11(6):246-51. doi: http://dx.doi.org/10.13175/swjpcc147-15 PDF

Ultrasound for Critical Care Physicians: 50 Ways to Line Your Liver

Seth Skiles ACNP

Theresa Heynekamp MD MPH

Division of Pulmonary, Critical care and Sleep Medicine,

University of New Mexico School of Medicine

Albuquerque, NM USA

A 54-year-old man with a past medical history significant for traumatic brain injury and aspiration pneumonia presented with hypoxic respiratory failure secondary to foreign body aspiration.

On presentation, the patient was found to be hypoxic and tachypneic, requiring endotracheal intubation and mechanical ventilation. Bronchoscopy was performed with removal of extensive food particles throughout both lungs. The patient subsequently developed sepsis secondary to aspiration pneumonia.  He became hypotensive, requiring central venous catheter placement for vasopressor therapy. A right subclavian central line was attempted under ultrasound guidance. A beside ultrasound was subsequently performed (Video 1).

Video 1. Sagittal view of the liver and heart at the level of the mid-abdomen and slightly right of mid-line.

What does the video obtained of a longitudinal view of the IVC at the level of the liver demonstrate? (Click on the correct answer for a discussion)

1. Endocarditis
2. Guidewire in the hepatic vein
3. Hemopericardium
4. Pneumothorax

Cite as: Skiles S, Heynekamp T. Ultrasound for critical care physicians: 50 ways to line your liver. Southwest J Pulm Crit Care. 2015;11(5):235-7. doi: http://dx.doi.org/10.13175/swjpcc144-15 PDF

November 2015 Critical Care Case of the Month

Samir Sultan, DO

Banner University Medical Center Phoenix

Phoenix, AZ

 History of Present Illness

A 39-year-old Caucasian woman was admitted to the ICU with worsening dyspnea and increasing oxygen requirements. Her lips turned blue with minimal activity. She was admitted to another hospital 5 months earlier with pneumonia. At discharge she was placed on oxygen. At follow-up with her pulmonologist, she was diagnosed with sleep apnea.

Past Medical History, Family History, Social History

• She has a history of an optic glioma at age 7 with resection followed by radiation therapy and development of panhypopituitarism.
• Liver cirrhosis diagnosed in 2014 with presentation of hematemesis.
• Type 2 diabetes mellitus
• Denies tobacco, ethanol, or illicit drug use.
• There is a family history of diabetes and liver cirrhosis

Physical Examination

• Vital signs:110 / 86, HR 97, RR 16, 88% on 6 liter O2
• General: obese female (BMI 35) in no apparent distress
• Chest: Clear to auscultation bilaterally
• Cardiovascular: regular rate without murmur or rub
• The remainder of the physical exam is normal  

Radiography

      A chest x-ray was interpreted as normal.

Laboratory

• CBC: hemoglobin 13.8 gm/dL, WBC 7 X 103 cells/microliter with a normal differential
• Basic metabolic panel: Na⁺ 132 mEq/L, K⁺ 4 mEq/L, Cl^- 100 mEq/L, HCO3^- 22 mEq/L, glucose 150 mg/dL.
• Arterial blood gases (ABGs): PaO₂ 35 mm Hg, PaCO₂ 37 mm Hg, pH 7.43

Which of the following is/are not possible cause(s) of hypoxemia in this patient? (Click on the correct answer to proceed to the second of six panels)

1. Decreased diffusion (alveolar capillary block)
2. Ventilation-perfusion mismatch
3. Hypoventilation
4. 1 and 3
5. All of the above

Cite as: Sultan S. November 2015 critical care case of the month. Southwest J Pulm Crit Care. 2015;11(5):209-15. doi: http://dx.doi.org/10.13175/swjpcc137-15 PDF

Ultrasound for Critical Care Physicians: The Martian

Jawad Abukhalaf, MD

Michel Boivin, MD

Division of Pulmonary, Critical care and Sleep Medicine,

University of New Mexico School of Medicine

Albuquerque, NM USA

A 54 year old male with a past medical history significant for granulomatosis with polyangiitis (formerly known as Wegener’s granulomatosis) and chronic kidney disease presented with hemoptysis and chest pain.

On presentation, he was found to have a 10 cm right middle lobe cavitary lesion and was subsequently treated with high dose steroids, antibiotics and antifungals based on bronchoalveolar lavage results. On day 9 of his hospital stay the patient was found to have bilateral lower extremity deep venous thromboses that were treated with intravenous heparin. On day 11 of his stay, the patient started experiencing lower abdominal pain and hypotension. The patient was resuscitated with saline. Bedside ultrasonography was performed.

Figure 1. Transverse lower abdominal ultrasound in the pelvis.

What does the transverse view of the lower abdomen (just above the symphysis pubis) demonstrate? (Click on the correct answer for an explanation)

1. Abdominal wall hematoma
2. Distended bladder
3. Horseshoe kidney
4. Psoas hematoma

Cite as: Abukhalaf J, Boivin M. Ultrasound for critical care physicians: the martian. Southwest J Pulm Crit Care. 2015;11(4):186-8. doi: http://dx.doi.org/10.13175/swjpcc135-15 PDF 

October 2015 Critical Care Case of the Month: A Moldy But Gooey

Jennifer M. Hall, DO

Banner University Medical Center Phoenix

Phoenix, AZ

History of Present Illness

A 45-year-old man with a history of a kidney transplant in 2011 was admitted with subjective fevers, nausea, abdominal pain, chest pain and recurrent renal failure. Cardiac workup was negative for ischemia and intermittent hemodialysis was initiated. CT of chest and abdomen was significant for a new cavitary pulmonary lesion. Leading up to this admission, he had been on immunosuppressive agents including tacrolimus, mycophenolate and prednisone, and the day of presentation had been doing quite well, actually was bear hunting in the mountains near Flagstaff, Arizona.

Past Medical History

• Donor kidney transplant in 1999, which failed in 2011, prompting a second kidney transplant
• Failed pancreas transplant
• Coronary artery disease, with percutaneous cardiac intervention in 2001
• Diabetes mellitus type I
• Chronic anemia
• History of total parathyroidectomy
• History of C5-C7 cervical fixation

Physical Examination

• Vital signs stable
• Appeared to be pale, no apparent distress
• Cardiac exam unremarkable
• Chest exam with fine crackles in left base / otherwise clear
• Abdomen slightly tender in left lower quadrant, but without guarding, rebound or peritoneal signs; small dime-sized area of ecchymosis, where lovenox injections had been administered
• No peripheral edema or clubbing

Laboratory Evaluation

• WBC 17,900 cells/mcL with 96% segmented neutrophils, hemoglobin 8.9 g/dL(after transfused 2 units prior to transfer), PLT 232,000 cells/mcL,
• INR 1.3
• Blood urea nitrogen (BUN) 74 mg/dL, serum creatinine 2.32 mg/dL, electrolytes within normal limits, albumin 3.2 g/dL, aspartate aminotransferase (AST) 24 IU/L, alanine transaminase (ALT)81 IU/L.
• NT-proBNP 6841 pg/ml (normal < 300 pg/ml)
• Hemoglobin A1C 7.2%
• Lactate 0.7 mmol/L

Imaging

A thoracic CT scan was performed (Figure 1).

Figure 1. Panels A-D: representative static views from the CT scan in lung windows. Note the cavitary lesion in the right lung (red arrow), the right pleural effusion (blue arrow) and the left lower lobe consolidation (yellow arrow) with a pleural effusion. Lower panel: video of the thoracic CT scan in lung windows.

Which diagnosis is least likely in this patient’s differential diagnosis for the cavitary pulmonary lesion? (Click on the correct answer to proceed to the second of five panels)

1. Aspergillosis
2. Coccidioidomycosis
3. Invasive mucormycosis
4. Metastatic malignancy
5. Nocardiosis
6. Pulmonary Infarct

Cite as: Hall JM. October 2015 critical care case of the month: a moldy but gooey. Southwest J Pulm Crit Care. 2015;11(4):136-43. doi: http://dx.doi.org/10.13175/swjpcc130-15 PDF

Ultrasound for Critical Care Physicians: Shortness of Breath

Matthew JK Douglas, MD

David Verbunker, MD

Jarrod Mosier, MD 

Department of Emergency Medicine

Banner University Medical Center Tucson

University of Arizona

Tucson, AZ

Figure 1. Video of the right thoracic ultrasound (coronal).

An 85 year old woman with a history of congestive heart failure and diabetes presented to the emergency department with progressive shortness of breath. She had recently been discharged from another hospital where she had been admitted for several days for community acquired pneumonia. The patient was in respiratory distress on arrival with tachypnea, increased work of breathing, and hypoxia despite supplemental oxygen with a non-rebreather mask and she was subsequently intubated. ED point-of-care ultrasound was performed of the right hemithorax.

What does Figure 1 demonstrate? (Click on the correct answer for the second of two panels and an explanation)

1. Intravascular volume depletion
2. Normal lung aeration
3. Numerous B-lines
4. Pleural effusion and consolidation
5. Pneumothorax

Cite as: Douglas MJK, Verbunker D, Mosier J. Ultrasound for critical care physicians: shortness of breath. Southwest J Pulm Crit Care. 2015;11(3):112-3. doi: http://dx.doi.org/10.13175/swjpcc116-15 PDF

September 2015 Critical Care Case of the Month: If You Don't Look, You Won't Find

Robert A. Raschke, MD

Banner University Medical Center

Phoenix, AZ

 History of Present Illness

A 55-year-old woman was transferred from Mexico emergently for acute cardiomyopathy. On the day of admission, she went for a 45-min “exercise” walk and cleaned her house. While taking a shower, she suffered an acute onset of dyspnea with nausea and vomiting and possibly a small amount of hematemesis. She appeared seriously ill to her husband, who took her blood pressure (198/?) and pulse (90) and rushed her to a local medical facility.  There, she was found to have severe pulmonary edema, and a troponin of 11.  Her echo showed inferior wall motion abnormality with an ejection fraction of 35%.  However, coronary catheterization showed normal coronaries.  She was treated with oxygen, furosemide, labetolol and enoxaparin and transferred emergently to Banner-University Medical Center. 

Past Medical History, Family History and Social History

The patient reported intermittent "spells" since May. These typically occurred upon  lying down in bed and were characterized by her as a feeling of “numbness” or tingling  which ascends from her chest to her head associated with palpitations and a feeling of  “desperation”, typically relieved after a few minutes upon getting up out of bed.

She had a history of hypertension and had been on losartan but this was discontinued a few months previously because of the onset of orthostatic dizziness. She also has a history of hypothyroidism and is taking synthroid. She was treated three times in the last 6 month for amoebiasis. She is a medical missionary to La Paz, Mexico and has recently traveled to Bolivia and Guatemala.

Review of Systems

She has had some night sweats, coughing with deep inspiration, and some slight hemoptysis. She did have a headache one month previously at 7000 ft elevation while in Guatemala.

Physical Examination

• She appears in moderate distress. Her vital signs are normal other than a mild tachycardia.  
• She does have rales on auscultation of her lungs.
• The remainder of the physical examination was unremarkable.

Radiography

A portable chest radiograph is performed (Figure 1).

Figure 1. Admission portable chest radiograph.

Laboratory evaluation

Her CBC shows a normal hemoglobin and hematocrit but with an elevated white blood cell count of 26,500 cells/mcL with a left shift. Admission electrolytes and blood sugar are within normal limits.

What additional procedures/testing are indicated? (Click on the correct answer to proceed to the second of four panels)

1. Blood cultures
2. Echocardiogram
3. Electrocardiogram
4. NT-pro-brain natriuretic peptide (NT-pro-BNP)
5. All of the above

Reference as: Raschke RA. September 2015 critical care case of the month: if you don't look, you won't find. Southwest J Pulm Crit Care. 2015;11(3):97-102. doi: http://dx.doi.org/10.13175/swjpcc113-15 PDF 

August 2015 Critical Care Case of the Month: A Diagnostic Branch of Medicine

William T. Love, MD

Karen L. Swanson, DO

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

 History of Present Illness

A 66-year-old man had undergone an orthotopic heart transplantation on March 28th, 2015 due to end-stage cardiomyopathy. During a recent hospitalization from 6/26-7/2 a transbronchial lung biopsy was suggestive of  subacute rejection. He was treated with:

• Plasmapheresis x 3
• Intravenous immunoglobulin (IVIG)
• 500 mg Solu-Medrol daily
• Tacrolimus held as supra-therapeutic level of 16.2
• Mycophenolate decreased to 500mg BID
• Prednisone at 10mg BID on discharge

On July 3rd he began having cough productive of clear sputum, nausea, vomiting, and headache. Subsequently he had body aches, subjective fever, chills, night sweats, and a poor appetite with a 4 kg weight loss over the last week. There was also a history of several falls after “losing his balance".

Past Medical History

There was also a history of type 2 diabetes mellitus, chronic kidney disease, coronary artery disease with coronary artery bypass grafting in 2000.

Physical Examination

• Vital signs: T-37.1, HR-100, BP-130/88, RR-22, 96% RA
• Heart: regular rate & rhythm. 2/6 Systolic Murmur
• Lungs: clear to auscultation bilaterally

Laboratory

• Hemoglobin 9.7, WBC 6.3, creatinine 2.2, mildly elevated AST/ALT
• Lumbar Puncture– Protein 58 mg/dL, Glucose 46 mg/dL, 47 Nucleated cells

Radiography

A chest x-ray was performed (Figure 1).

Figure 1. Admission PA of the chest.

Based on the chest x-ray and lumbar puncture, which of the following are true? (Click on the correct answer to proceed to the second of four panels)

1. The chest x-ray and lumbar puncture findings in this clinical situation suggest cancer metastatic to the lung and brain
2. The chest x-ray and lumbar puncture findings in this clinical setting suggest an infection involving the lung and brain
3. The clinical findings suggest granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis)
4. The clinical findings are suggestive of acute rejection
5. The clinical findings are suggestive of tuberculosis

Reference as: Love WT, Swanson KL. August 2015 critical care case of the month: a diagnostic branch of medicine. Southwest J Pulm Crit Care. 2015;11(2):59-65. doi: http://dx.doi.org/10.13175/swjpcc100-15 PDF

Ultrasound for Critical Care Physicians: Take a Deep Breath

David Ling, DO

Michel Boivin, MD

Division of Pulmonary, Critical care and Sleep Medicine

University of New Mexico School of Medicine

Albuquerque, NM

A 40 year old man with a past medical history of intravenous drug abuse presented to the emergency department with difficulty walking and lower extremity weakness. He did admit to recent heroin use. He became somnolent in the ED and was given naloxone. However, he did not improve his level of consciousness sufficiently and was intubated for hypercarbia. The patient was transferred to the MICU and was evaluated for respiratory failure. He later that day passed a spontaneous breathing trial after he awoke and was extubated. However, he was soon thereafter was re-intubated for poor respiratory efforts and a weak cough. 

With an unexplained etiology for the respiratory failure, CT of the head, MRI of the brain and lab evaluation were pursued but were negative.  At that point, a bedside ultrasound of the right hemi-diaphragm in the zone of apposition was obtained and is shown below:

Figure 1. Ultrasound of the right hemi-diaphragm at low depth, at the zone of apposition. The diaphragm is visualized above the liver as three parallel echogenic stripes.

Figure 2. M-mode image of the right hemi-diaphragm. The m-mode image is on the left, and the corresponding 2D image is on the right.

What does the video and M-mode of the diaphragm demonstrated above predict for the potential result of the patient’s extubation? (Click on the correct answer for the answer and explanation)

1. Success
2. Failure
3. Has no predictive value

Reference as: Ling D, Boivin M. Ultrasound for critical care physicians: take a deep breath. Southwest J Pulm Crit Care. 2015;11(1):38-41. doi: http://dx.doi.org/10.13175/swjpcc091-15 PDF

July 2015 Critical Care Case of the Month: An Unusual Presentation

Allon Kahn, MD 

Lewis J. Wesselius, MD
 

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

History of Present Illness

A 79 year old man was admitted because of a possible seizure. His wife found him unresponsive, displaying tonic-clonic motions with a right facial droop and right-sided weakness. He returned to consciousness, but was confused. A similar episode occurred 2 weeks prior to the present episode. He has additional symptoms of dysphagia with solid food for 6-8 months, a somewhat intentional 20 pound weight loss, night sweats for 4-5 months and fatigue for 1 year.

Past Medical History

• Coronary artery disease with a percutaneous transluminal coronary angioplasty in 1990, placement of 2 drug eluting stents in 2012.
• Idiopathic pulmonary fibrosis on 2-4 L/min home O2
• Myelofibrosis on ruxolitinib, a monoclonal antibody against JAK receptors
• Hypertension
• A remote history of DVT/PE related to surgery with an IVC filter placed
• Splenectomy due to trauma

Social and Family History

• He has a 15 pack-year smoking history, quitting in 1985.
• One brother with lung cancer, another with bladder cancer.

Medications

• Aspirin 81 mg daily
• Plavix 75 mg daily
• HCTZ 25 mg daily
• Metoprolol XL 50 mg daily
• Niacin 500 mg daily
• Protonix 40 mg daily
• Acetaminophen with hydrocodone
• Fish oil

Physical Examination

• Dysarthric
• No facial droop
• Some dysmetria

Which of the following should be done at this time? (Click on the correct answer to proceed to the second of five panels)

1. A CT scan of the brain
2. Begin tissue plasminogen activator (TPA)
3. Chest x-ray
4. 1 and 3
5. All of the above

Reference as: Kahn A, Wesselius LJ. July 2015 critical care case of the month: an unusual presentation. Southwest J Pulm Crit Care. 2015;11(1):11-18. doi: http://dx.doi.org/10.13175/swjpcc086-15 PDF

June 2015 Critical Care Case of the Month: Just Ask the Nurse

Robert A. Raschke, MD

Banner University Medical Center

Phoenix, AZ

 History of Present Illness

A 61-year-old police officer had just finished delivering a speech at a law enforcement conference in Phoenix when he briefly complained of chest pain or chest tingling before lapsing into a mute state. He became diaphoretic cyanotic, and vomited. Emergency medical services was called. They noted a blood pressure of 80/50 mm Hg, a pulse of 45, temperature of 95º F, a respiratory rate of 12, and widely dilated pupils. He was transported to the emergency room.

PMH, SH, FH, Medications

Unknown.

Physical Examination

Vital signs: blood pressure 120/75 mm Hg by oscillometric thigh cuff, pulse 43 and irregular, temperature 96º F, respiratory rate 10, SpO2 96% on O2 @ 5L/min by nasal cannula

Neck: No JVD.

Lungs: Poor inspiratory effort

Heart: Irregular rhythm without a murmur

Neurological:

• Delirious – mute – won’t obey commands or track with his eyes
• Pupils 3 mm reactive
• Withdrew 3 extremities to nail bed pressure – he will defend his left arm with his right arm

He suddenly became asystolic and cardiopulmonary resuscitation was begun. After about a minute a femoral pulse could be felt.

Which of the following are indicated at this time? (Click on the correct answer to proceed to the second of five panels)

1. Arterial blood gas
2. Chest x-ray
3. Electrocardiogram
4. Electrolytes
5. All of the above

Reference as: Raschke RA. June 2015 critical care case of the month: just ask the nurse. Southwest J Pulm Crit Care. 2015;10(6):323-9. doi: http://dx.doi.org/10.13175/swjpcc077-15 PDF

Acute Pregabalin Withdrawal: A Case Report and Review of the Literature

Jaclyn A. Barrett, PharmD

Lindsay M. Kittler, PharmD, BCPS

Clement Singarajah, MD, FCCP

Phoenix VA Medical Center

Phoenix, AZ 85012

Abstract

Objective: Pregabalin is a commonly prescribed GABA analog most commonly used for the treatment of neuralgia. Recently, case reports on pregabalin have been published describing episodes that may be associated with withdrawal-like symptoms after extended or aggressive therapy. This report describes a case in which long term exposure of high dose pregabalin may have resulted in acute withdrawal, and outlines the subsequent medical management of these symptoms.

Case Summary: A 61-year-old male presenting with severe agitation presumed to be withdrawal from long term and high dose exposure to pregabalin. Medical management included the use of haloperidol, diphenhydramine, lorazepam and the addition of clonidine over the course of several days for the pharmacological management of withdrawal symptoms.

Discussion: Although case reports are available to guide clinicians in the recognition of acute pregabalin withdrawal, definitive evidence on how best to treat these patients remains severely limited. With an increase in the prescribing practices of pregabalin, insight into the acute management by fellow clinicians is further needed.

Conclusion: Caution must be practiced when prescribing and educating patients on the use of pregabalin to prevent associated withdrawal-like symptoms. In addition, documentation by the medical community on methods utilized to treat pregabalin withdrawal syndromes remains crucial for the advancement of patient care. Benzodiazepines and clonidine are the current therapies that have been documented as potentially effective treatment modalities at this time.

Introduction

Pregabalin is a gamma-aminobutyric acid (GABA) analogue currently FDA labeled for diabetic peripheral neuropathy, fibromyalgia, neuropathic pain, partial seizures and postherpetic neuralgia, and is used off-label in various psychiatric disorders. It is proposed that pregabalin binds strongly to an alpha-2-delta subunit on voltage gated calcium channels within the central nervous system. Pro-nociceptive neurotransmitter release that is dependent upon calcium is thereby reduced. Additional mechanisms for pregabalin’s efficacy may be comprised of noradrenergic and serotonergic pathways involved in pain transmission (1).

Case Presentation

We report the case of a 61-year-old man who presented with sudden and severe withdrawal like symptoms characterized by family as extreme agitation with combative behavior, diaphoresis, tachycardia, hypertension, tremors, and incontinent diarrhea. Reportedly, prior to admission, the patient had become increasingly somnolent with multiple falls and psychotic behavior similar to one responding to internal stimuli. A review of his home prescription vials revealed a presumed, excessive consumption of immediate-release oxycodone and pregabalin over the last few days and up to a week. His past medical history included chronic obstructive pulmonary disease, osteoarthritis, neuropathic pain, hypothyroidism, hyperlipidemia, anxiety and major depressive disorder. A thyroid stimulating hormone level was checked upon admission and was within normal limits with no other metabolic explanation for his symptoms identified. The patient did present with a prior medical history of opioid abuse with previous enrollments in substance abuse programs, but compliance with his current pain management contract was confirmed using the state’s controlled substance prescription monitoring program database.

Upon admission through the emergency room, the patient remained severely agitated with increasingly combative behavior despite the administration of the antipsychotic, haloperidol. Without relief, the benzodiazepine, lorazepam, was administered resulting in a paradoxical effect causing increased aggression and agitation and thus discontinued. Implementation of scheduled hydromorphone was administered for acute opioid withdrawal but similarly provided minimal symptom abatement yet, maintained adequate analgesia. After medication review and reconciliation, the patient was currently on a prescribed, scheduled dose of pregabalin 300 mg twice daily over the course of approximately eight months for the treatment of neuropathic pain. Although initially concerned for potential overdose, all symptoms upon presentation were deemed to be consistent with a withdrawal syndrome, pregabalin being the most likely culprit given lack of symptom abatement with the use of benzodiazepines and opioids with no other likely cause upon review of his home medications and laboratory data.

After transferring to the Intensive Care Unit, the patient was further treated with intravenous haloperidol 10 mg and diphenhydramine 50 mg every 4 hours providing only minimal relief while protecting both the safety of the patient and staff. Management of acute pregabalin withdrawal was further complicated by the inability to provide pregabalin orally, due to disorientation and the physical inability to maintain placement of a nasogastric tube. Sedation and mechanical ventilation was not an option as the patient’s established wishes were a Do Not Intubate (DNI) status. Sublingual clonidine 0.1 mg was later administered every four hours and up to every hour if needed, in addition to the haloperidol and diphenhydramine. The anti-adrenergic agent clonidine was most effective in providing withdrawal symptom reduction, and the haloperidol and diphenhydramine were rapidly tapered off. In addition, our patient developed urinary retention necessitating the discontinuation of diphenhydramine. The discontinuation of diphenhydramine lead to a retrial of lorazepam which provided effective relief for the management of his later course agitation with no paradoxical agitation observed.

This case demonstrates an issue of common occurrence, where a patient is withdrawing clinically from a drug with often non-specific symptom manifestations. Further confounding this clinical presentation, several possible sources of drug withdrawal required the medical team to address each drug individually in order to identify the offending agent. With this in mind, withdrawal from pregabalin, although not often considered a drug of abuse or associated with intense withdrawal, may only be identified by ruling out other suspected agents, such as in this patient scenario.

Discussion

In review of current literature, case reports have arisen that describe symptoms of withdrawal from abrupt discontinuation of pregabalin. Several case reports describe a withdrawal-like syndrome to include signs and symptoms such as agitation, anxiety, confusion, gastrointestinal distress, tachycardia and palpitations, similar to benzodiazepine withdrawal (2-4).

Oaklander and Buchbinder (2) report a case involving an 80-year-old woman prescribed pregabalin 125 mg three times daily for 49 weeks as treatment for postherpetic neuralgia. Within 36 hours of abrupt discontinuation, the patient developed severe nausea, headache, imbalance, delirium and anorexia. Over the course of several weeks, the patient developed hemodynamic instability and continued to experience episodes of ataxia for a six month duration.

Another report by Karosin et al. (3), describes a 47-year-old male who reportedly consumed a total daily dose of 7,500 mg of pregabalin daily in addition to alcohol and cocaine abuse. In a failed attempt to wean off pregabalin the patient developed what was described to be vegetative withdrawal symptoms, sweating, restlessness, hypertension, tremor and pregabalin cravings. Upon admission, the patient received treatment with benzodiazepines without relief and a slow taper of pregabalin was initiated yet, cravings continued which ultimately resulted in the patients continued abuse of this GABA analog.

In a case report by Norgaard et al. (4), a 38 year-old man was self-administering 8.4 g pregabalin daily and within 36 hours of cessation of pregabalin developed auditory hallucinations and suicidal ideation in addition to sweating, anxiety and tachycardia. Pregabalin was reinitiated at 600 mg per day in addition to supplemental chlordiazepoxide and quetiapine. Acute symptoms resolved within 48 hours yet the symptoms of psychosis remained present until several weeks after discontinuation.

In addition, case reports regarding gabapentin withdrawal have been published to include similar clinical presentations. Gabapentin, another GABA analog, is FDA approved for the treatment epilepsy, neuralgia and restless leg syndrome, and is widely used in the prophylaxis of migraines, headaches and ethanol withdrawal (5). It is hypothesized that the mechanism of withdrawal is associated with increased activity of the enzyme responsible for producing GABA, similar to the mechanism behind ethanol and benzodiazepine withdrawal (6).

Hellwig et al. (6) and Mah et al. (7), describe similar symptoms of irritability, confusion and agitation unrelieved by the administration of benzodiazepines. Gabapentin was identified as the causative agent of withdrawal after reinstatement of the GABA analog provided relief in both case reports. In addition to drug related factors, potential patient related risk factors that may increase the susceptibility of withdrawal include advanced age and history of psychiatric illness.

Currently, pregabalin is a schedule V controlled substance due to its potential for addiction and abuse (8). According to the manufacturer, there are no current recommendations for the management of an acute drug withdrawal syndrome from pregabalin, yet current practice suggests that a gradual taper, generally recommended with all extended controlled substance therapy, may be warranted. This report suggests that clonidine may be an effective agent in the management of acute agitation associated with pregabalin withdrawal. Literature has historically supported the use of clonidine in a variety of drug withdrawal syndromes owing to its known central alpha 2 agonist activity, but remains underutilized amongst providers in current practice (9-11). Another alternative to consider is dexmedetomidine, a centrally acting, alpha 2 adrenoceptor agonist which has demonstrated its efficacy as an adjunctive treatment for refractory alcohol withdrawal (12). Due to concomitant hypertension and institutional cost, dexmedetomidine was considered second line in the event that clonidine was ineffective for our patient.

Although case reports are available to guide clinicians in the recognition of acute pregabalin withdrawal, definitive evidence on how best to treat these patients remains severely limited. With an increase in the prescribing practices of pregabalin, insight into the acute management by fellow clinicians is further needed to provide evidence-based guidance in the management of these patients. As for our clinical case of acute pregabalin withdrawal in the presence of hallucinatory features, we advise against the use of benzodiazepines due to the risks of paradoxical agitation, and would suggest withholding their use until the latter stages of withdrawal. If possible, as was not in our case, initiating a pregabalin taper would ideally preferred. We also propose that the use of clonidine has clinically shown, as demonstrated in this patient case, to provide appropriate supportive treatment for the management of acute pregabalin withdrawal.

References

1. Pregabalin. DrugPoint Summary. Micromedex. Truven Health Analytics, Inc. Greenwood Village, CO. Available at: http://www.micromedexsolutions.com. Accessed April 26, 2014.
2. Oaklander AL, Buchbinder BR. Pregabalin-withdrawal encephalopathy and splenial edema: a link to high-altitude sickness? Ann Neurol. 2005;58(2):309-12. [CrossRef] [PubMed]
3. Karosin C, Kofler M, Mayr A, et al: Pregabalin: A treatment option for dystonia? Neurol Sci. 2012;33(2):351-4. [CrossRef] [PubMed]
4. Nordgaard J, Jurgens G. A case of pregabalin abuse. Clin Toxicol. 2013;51(4):320
5. Gold Standard, Inc. Gabapentin. Clinical Pharmacology [database online]. Available at: http://www.clinicalpharmacology-ip.com/Forms/drugoptions.aspx?cpnum=271&n=Gabapentin&t=0 Accessed: 5/19/2015.
6. Hellwig TR, Hammerquist R, Termaat J. Withdrawal symptoms after gabapentin discontinuation. Am J Health Syst Pharm. 2010;67:910-2. [CrossRef] [PubMed]
7. Mah L, Hart M. Gabapentin withdrawal: case report in an older adult and review of the literature. J Am Geriatr Soc. 2013;61(9):1635-7. [CrossRef] [PubMed]
8. LYRICA® (pregabalin) CV Safety Info. Available at: http://www.lyrica.com. Accessed April 27, 2014.
9. Baumgartner GR, Rowen RC. Clonidine vs chlordiazepoxide in the management of acute alcohol withdrawal syndrome. Arch Intern Med. 1987;147:1223-6. [CrossRef] [PubMed]
10. Baumgartner GR, Rown RC. Transdermal clonidine versus chlordiazepoxide in alcohol withdrawal: a randomized, controlled clinical trial. South Med J. 1991;84:312-21. [CrossRef] [PubMed]
11. Robinson BJ, Robinson GM, Mailing TJB, Johnson RH. Is clonidine useful in the treatment of alcohol withdrawal? Alcohol Clin Exp Res. 1989;13:95-8. [CrossRef] [PubMed]
12. Tolonen J, Rossinen J, Alho H, Harjola VP. Dexmedetomidine in addition to benzodiazepine-based sedation in patients with alcohol withdrawal delirium. Eur J Emerg Med. 2013;20:425. [CrossRef] [PubMed]

Reference as: Barrett JA, Kittler LM, Singarajah C. Acute pregabalin withdrawal: a case report and review of the literature. Southwest J Pulm Crit Care. 2015;10(5):306-10. doi: http://dx.doi.org/10.13175/swjpcc059-15. PDF

Organ Failure in Acute Pancreatitis and Its Impact on Outcome in Critical Care

Namrata Maheshwari, MD, IDCCM

Arun Kumar, MD 

Zafar A Iqbal, MD

Amit K Mandal, DNB,DTCD

Abhishek Vyas, MBBS

Jai D Wig, MS

Department of Critical Care Medicine and Pulmonology

Fortis Hospital 

Mohali, Punjab, 160062

India 

Abstract

The most important determinant of mortality in acute pancreatitis is organ failure (OF). The aim of this prospective observational study was to determine the incidence of organ failure in acute pancreatitis and its relation with the extent of necrosis and outcome. Sixty-one patients were divided into 3 groups: no organ failure (NOF), transient organ failure (< 48 hrs) (TOF) or persistent organ failure (> 48 hrs) (POF). Of 61 patients, 30 patients had no organ failure (49.1%), while 11 patients (18%) had TOF and 20 patients (32.7%) had POF. The mean age was 46.5 yrs with male predominance. Pulmonary and renal failures were the most common (32%), followed by CVS (cardiovascular system), coagulation system and CNS (central nervous system). Fourteen (46.4%) patients had one or two OF, 17 (56.6%) had more than two OF. There were no deaths in patients with up to two organ failures but a 70% (7) death rate in those with three organ involvement, 80% (4) with four and 100% with five OF. The percentage of pancreatic necrosis was evaluated for its relationship with organ failure. In the NOF group 19 (63.3%) patients had no necrosis, as compared to 11 patients with necrosis in TOF and POF groups (35.4%). Out of 61 patients, 13 patients died. All 13 patients who expired belonged to the POF group (p <.001). Early persisting and deteriorating organ failure had the worst outcomes. There was an increase in mortality with an increasing number of organs involved. The extent of necrosis was directly related with incidence of organ failure.

Introduction

Acute pancreatitis (AP) is characterized by a variable clinical course varying from a mild self-limited disease (80-90%) to a clinically severe acute pancreatitis (SAP) in 10-20% (1-4). Despite advances in knowledge and treatment of AP, the identification of patients with clinically severe disease on admission remains difficult (1) and the mortality in several series continues to be around 20% (2,5). 

The factors responsible for high mortality in patients with SAP are organ failure (OF) and pancreatic necrosis (6,7). The reported incidence of OF in SAP varies from 28-76 % (5,8,9). The occurrence of organ dysfunction and progressive organ failure has a major impact on outcome. Many patients who succumb to AP within the first two weeks of disease onset do so from overwhelming multiorgan failure (10,11). Other studies have also reported that prognosis deteriorated with an increase in number of organs involved (12,13). Banks and Freeman (14) studied the correlation between mortality and organ failure in patients with acute pancreatitis and documented a median mortality of 3% in patients with single organ failure and 47% in patients with multisystem organ failure. Another study documented that the overall mortality (47.8%) correlated with the number of organs failing (6). The definition of multiorgan failure is broad and encompasses transient to persistent or severe multiorgan failure that requires critical care support (15). Patients with persistent organ failure have a higher mortality as compared to patients where organ failure resolves (16). Johnson and Hial (17) showed that patients with OF that resolved within 48 hours(transient) have a low risk of complications and death in comparison to patients who have persistent organ failure(OF persisting for 3 or more days) and have a greater than one in three risk of fatal outcome. Information regarding the prediction of persistent organ failure in patients with acute pancreatitis is not available (18).

One of the factors linked to the development of OF is the extent of pancreatic necrosis. Some workers have found a correlation between the extent of necrosis and OF (19). The question of the relationship between infected necrosis and OF remains unsettled. There is no consistency in the literature on whether organ failure or infected necrosis is the main determinant of severity in acute pancreatitis. The aim of study was to study the occurrence of organ failure in acute pancreatitis and determine the influence of organ failure on mortality in patients with acute pancreatitis.

Materials and Methods

This study was a prospective study under taken during 18 months (December 2011 to May 2013) in the Departments of Gastroenterology, General Surgery and Medical Intensive Care Unit in Fortis Hospital, Mohali, Punjab, a 260 bedded multispecialty tertiary care hospital in Northern India.

The study sample included all consecutive patients diagnosed with acute pancreatitis referred to Gastroenterology or General surgery units fulfilling the inclusion and exclusion criteria. All the patients were assessed for demographic profile and detailed symptom profile. After a detailed clinical examination relevant investigations were repeated as and when required. Patients were monitored for the presence and severity of organ failure every day during the first week, subsequent local complications, subsequent episodes of sepsis, and death or other outcomes during the same hospital admission.

Organ failure was defined as per modified multiple organ failure score (MMOFS). Transient organ failure was defined as organ failure present for less than 48 hours, and persistent organ failure was recorded when organ failure was present for more than 48 hours, where day 0 was the day of entry to the study and day one started at 8.00am on the day after entry. The course in hospital and final outcome was recorded. Cross tabulations were made with outcome, in particular with mortality.

Statistical Analysis. The data are presented as mean ± SD or median and interquartile range, as appropriate. The Mann- Whitney U-test was used for statistical analysis of skewed continuous variables and ordered categorical variables. For normally distributed data The t-test was applied. Pearson χ2 test or Fisher’s exact test was used for analysis of categorical variables with two categories. A p value of <0.05 was considered to indicate statistical significance. All calculations were performed using SPSS® version 15 (Statistical Packages for the Social Sciences, Chicago, IL).

Results

The study was comprised of 61 patients who met the inclusion criteria with diagnosis of acute pancreatitis. The study group was further divided as per organ failure into three groups:

• No organ failure (NOF)
• Transient organ failure ( < 48 hrs) (TOF)
• Persistent organ failure ( > 48 hrs) (POF)

Demographic Distribution. The mean age of the patients was 46.5 years. The majority of patients were in the age group of 30-50 years. In this study the youngest patient was 17 years old and oldest was 87 years old (Figure 1).  

Figure 1. Age distribution with increased number of organs involvement.

The male to female ratio was found to be 2.4:1 (Figure 2).

Figure 2. Sex distribution.

Male predominance was found in all groups (53.3 %, 81.8%, and 90 % in the no organ, transient and persistent organ failure group respectively).

Comorbid Conditions. A majority of the patients (38) in our study group had no associated comorbid conditions  while 23 patients (37.8%) had a previous comorbid condition. Hypertension was the most common comorbid condition, seen in almost 31 % of the patients at the time of admission. Type 2 diabetes was the second most common condition noted in 24.6%, followed by hypothyroidism (4.9%), asthma, depression, cardiomyopathy and Guillain-Barré syndrome in 1.6% each (Table 1).  

Table 1. Comorbid conditions associated in our study group.

 

We could not find any association between co morbidities and mortality as 9 (62.9%) deaths occurred in the no comorbidity group as compared to 4 (30.8%) deaths in the co morbidities group (p=0.880).

Etiology. The most common etiologies of pancreatitis in our study group were alcohol and gall stones (n=24, 39% each) (Table 2).

Table 2. Etiology of acute pancreatitis.

Other causes were idiopathic (n=10, 17%), hypertriglyceridemia (n=2, 3%) and pancreatic divisum (n=1, 2%).

Percentage of Necrosis and Organ Failure. The percentage of necrosis on radiological imaging (in 46 patients) was evaluated for its relationship with organ failure. In the NOF group 19 (63.3%) patients had no necrosis (0%), 4 (13.3%) patients had <30% necrosis, 1 (3.3%) had 30-50% and 4 (13.3%) had >50% necrosis (Figure 3).

Figure 3. Relation between organ failure and pancreatic necrosis.

In the TOF group, 4 (36.4%) patients revealed no necrosis on contrast-enhanced computerized tomography (CECT) of the abdomen, <30% necrosis in 2 (18.2%) patients, 30-50% necrosis in 3 (27.3%) and >50% in 1 (9.1%) patient (Figure 3).

In POF group no necrosis was detected in 3 (15%) patients, <30 % in 2 (10%), 30-50% in 1 (5%) and >50% in 2 (10%) patients. The relationship between the amount of necrosis was directly related with incidence of organ failure and this correlation was found to be statistically significant (Figure 3).

MMOFS and Mortality. We divided our study in 3 groups, no organ failure, transient (<48 hrs) and persistent (>48 hrs) organ failure to understand the nature and dynamics of organ failure. Groups were further divided in early onset (<7days), late onset (>7days). Organ failure was calculated by the Modified multiorgan failure score (MMOFS). Daily MMOFS was calculated in all patients up to 7 days. MMOFS difference was calculated by MMOFS 7 (MMOFS at day 7) – MMOFS 1 (at the time of admission). On the basis of MMOFS difference groups were further divided into same (if difference was 0), improving (if deference was negative value), or deteriorating (if deference was a positive value) groups (Figure 4).

Figure 4. Comparison of outcome with MMOFS difference.

MMOFS difference was found to be highly significantly (ANOVA, p<0.001 each) correlated with organ failures and outcome. In our study no deaths occurred in the transient OF groups (early transient, late transient and transient deteriorating). We attributed this to the dynamics that transient OF could resolve with treatment and had a better outcome than persistent OF. Among the 13 deaths reported in our study, 46.2 % were in the early (<7 days) OF group compared to the late (>7 days) OF group (20%).

Organ Involvement. Pulmonary and renal failures were the most common organ involvements noted among our study group (32% each). This was followed by cardiovascular system (22%), coagulation system (8%) and central nervous system (6%) (Figure 5).

Figure 5. Organ failure by system.

Organ involvement and mortality. Fourteen (46.4%) patients had one or two OF and 17 (56.6%) had more than two OF (table 3). Comparison of the number of organ failures to mortality was statically significant (p<0.001) (Figure 6).

Figure 6. Outcome in patients with increasing organ involvement.

We found that there was an increase in incidence of mortality with an increase in the number of organs involved. There were no deaths in patients with up to two organ failures; it increased with increasing number of organs involved (Table 3).

Table 3. Organ failure and mortality.

The mortality rate was 70% (n=7) with three organ involvement, 80 % (n=4) with four and 100% with five OF.

Discussion

Severe acute pancreatitis is a systemic disease and characterized by acute onset and rapid progression, with a high incidence of complications and serious morbidity (20). An international multidisciplinary classification of acute pancreatitis severity is based on local and systemic determinants of severity. The local determinants relate to presence of pancreatic necrosis, and whether the necrosis is infected or sterile. The systemic determinants relate to whether there is organ failure or not, and if present, whether it is transient or persistent. The presence of both infected pancreatic necrosis and persistent organ failure has a greater impact on severity than either determinant alone. Based on these principles, the severity is classified as mild, moderate, severe or critical (21).The three most common systems involved are renal, lung, and cardiovascular system. Respiratory complications are frequent in acute pancreatitis and respiratory dysfunction is a major component of multiple organ dysfunction syndrome (22,23). In a population based study, 15.05% of patients with AP had a diagnosis of acute renal failure (24).

The present study showed that the difference in age was not significantly different between the groups. There are some studies which showed an association between advancing age as a predictor of organ failure and mortality. Wig et al. (6) studied 161 patients and concluded that age of the patients was a risk factor for multiple organ failure. Li et al. (25) studied 181 patients with SAP and found a correlation of age with OF (<.001). Frey et al²⁶ also showed that the number of complications was positively correlated with the age of patients. Older age and number of complications were strong predictors of organ failure among patients with SAP. Though we recorded a higher incidence of organ failures and mortality in a younger age group of 40-45, the difference was attributed to a small number of patients above 65 years in our study as compared to studies done in the western world.

The bedside index for severity in acute pancreatitis (BISAP) score represents a simple way to identify patients at risk for increased mortality and the development of intermediate markers of severity within 24 hours of presentation. In our series the BISAP score was significantly associated (p<.001) with organ failure as well as survival (p<.001). We found 9 out of 13 deaths in the >3 score group and four deaths at a BISAP score of 2 as compared to zero mortality in the BISAP score 1 and 0 group. Kim et al. (27) also compared BISAP, the serum procalcitonin (PCT), and other multifactorial scoring systems simultaneously, concluded that BISAP is more accurate for predicting the severity of acute pancreatitis than the serum procalcitonin, APACHE-II, Glasgow, and modified CT severity index (MCTSI) scores. Chen et al. (28) evaluated the accuracy of BISAP in predicting the severity and prognosis of acute pancreatitis (AP) in 497 Chinese patients. They conclude that BISAP score is valuable in predicting the severity of AP and prognoses of SAP in Chinese patients.

Contrast enhanced computed tomography (CECT) is considered the gold standard for the diagnosis of pancreatic necrosis and peripancreatic collections. CT assessment correlates with the clinical course of the disease and recognized variables of disease severity. We ordered CECT in all patients on the second or third day after admission rather than at the time of admission. Additional contrast-enhanced CT scans were ordered at intervals during the hospitalization to detect and monitor the course of intra-abdominal complications of acute pancreatitis, such as the development of organized necrosis, pseudocysts, and vascular complications including pseudoaneurysms. In our study CT severity index (CTSI) > 7 at admission did not correlate well with organ failure or mortality (p=NS), although the percentage of necrosis had significant correlation with organ failure. Our results are similar to many studies reported in the literature. Simchuk et al. (29) performed a study on 268 patients with acute pancreatitis. They concluded CTSI > 5 correlated significantly with death. Similar results were also obtained by Leung et al. (30) on 121 patients studied retrospectively, and they concluded that CTSI is superior to Ranson’s score and APACHE II score in predicting outcome in pancreatitis. However a few studies found no association between grade of necrosis and outcome of pancreatitis. Shinzeki et al. (31) did not find any correlation between necrosis evident on CECT at admission and outcome of SAP (p=0.061). Another study by Lankisch et al. (32) also did not find any correlation between necrosis and organ failure.

In our study pulmonary and renal were the most common organ failures observed (32% each). The total number of organ failures at admission was also significantly different in both groups (p=0.001), however none of the organ failures independently proved to be a significant predictor of mortality. MMOFS difference was found to be highly significantly correlated with organ failures and outcome. Among the 13 deaths reported in our study, 46.2 % were in the early (<7 days) OF group compared to the late (>7 days) OF group (20%). Our series also showed comparable results with other studies suggesting that early organ failure is the major predictor of poor outcome MMOFS difference was found to be highly significantly (ANOVA, p<0.001 each) correlated with organ failures and outcome. In our study no deaths occurred in the transient OF groups (early transient, late transient and transient deteriorating). We attributed this to the dynamics that transient OF could resolve with treatment and had a better outcome than persistent OF. Among the 13 deaths reported in our study, 46.2 % were in the early (<7 days) OF group compared to the late (>7 days) OF group (20%). Our series also showed comparable results with other studies suggesting that early organ failure is the major predictor of poor outcome (p=0.002) compared to late organ failure (p=0.400).

We found that early persistent OF had a 66.6% mortality as compared to persistent deteriorating organ failure which also had a very high mortality (72.2%). Very few studies have reported on the dynamics of OF with MMOFS. Johnson et al. (19) in a study of 290 patients with SAP had 116 patients with no OF and 147 patients with OF at the time of admission subdivided those with OF into those with persistent (OF lasting for>48 hours) and transient (OF lasting for<48hours) organ failure. Mortality was 36.3% in persistent and 5% in transient OF group. No patients without OF died.

On analysis of the 13 patients who expired, 4 patients died early (<7 days) and 9 deaths were late (>7 days). OF was the main cause of death in both groups, however all patients with sepsis died later. In the study of Yang et al. (33) the most important and common cause of death for patients with fulminant pancreatitis was multiple organ dysfunction syndrome, which usually was the consequence of systemic inflammation response syndrome in the early stage, and severe infection in the later stage, respectively.

Conclusions

Patients with persistent organ failure have a higher mortality. Early persisting and deteriorating organ failure had the worst outcome of among patients with acute pancreatitis. There was an increase in mortality with increasing number of organs involved. The extent of necrosis was directly related with the incidence of organ failure.

References

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5. Poves Prim I, Fabregat Pous J, García Borobia FJ, Jorba Martí R, Figueras Felip J, Jaurrieta Mas E. Early onset of organ failure is the best predictor of mortality in acute pancreatitis. Rev Esp Enform Dig (Madrid). 2004;96:705-13. [PubMed]
6. Wig JD, Bharathy KG, Kochhar R, Yadav TD, Kudari AK, Doley RP, Gupta V, Babu YR. Correlates of organ failure in severe acute pancreatitis. JOP. 2009;10:271-5. [PubMed]
7. Mole DJ, Olabi B, Robinson V, Garden OJ, Parks RW. Incidence of individual organ dysfunction in fatal acute pancreatitis: analysis of 1024 death records. HPB (Oxford). 2009;11:166-70. [CrossRef] [PubMed]
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9. Lytras D, Manes K, Triantopoulou C, Paraskeva C, Delis S, Avgerinos C, Dervenis C. Persistent early organ failure: defining the high-risk group of patients with severe acute pancreatitis? Pancreas. 2008;36:249-54. [CrossRef] [PubMed]
10. Vege SS, Gardner TB, Chari ST, Munukuti P, Pearson RK, Clain JE, Petersen BT, Baron TH, Farnell MB, Sarr MG. Low mortality and high morbidity in severe acute pancreatitis without organ failure: a case for revising the Atlanta classification to include moderately severe acute pancreatitis. Am J Gastroentrol. 2009;104:710-5. [CrossRef] [PubMed]
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13. Mofidi R, Duff MD, Wigmore SJ, Madhavan KK, Garden OJ, Parks RW. Association between early systemic inflammatory response, severity of multiorgan dysfunction and death in acute pancreatitis. Br J Surg. 2006:93:738-44. [CrossRef] [PubMed]
14. Banks PA, Freeman ML. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 2006;101:2379-2400. [CrossRef] [PubMed]
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16. de-Madaria E, Soler-Sala G, Lopez-Font I, Zapater P, Martínez J, Gómez-Escolar L, Sánchez-Fortún C, Sempere L, Pérez-López J, Lluís F, Pérez-Mateo M. Update of Atlanta classification of severity of acute pancreatitis: should a moderate category be included. Pancreatology. 2010;10: 613-9. [CrossRef] [PubMed]
17. Johnson CD, Abu-Hilal M. Persistent organ failure during the first week as a marker of fatal outcome in acute pancreatitis. Gut. 2004;53;1340-4. [CrossRef] [PubMed]
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24. Lin HY, Lai JI, Lai YC, Lin PC, Chang SC, Tang GJ.Acute renal failure in severe pancreatitis: a population based study. Ups J Med Sci. 2011;116:155-9. [CrossRef] [PubMed]
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27. Kim BG, Noh MH, Ryu CH, Nam HS, Woo SM, Ryu SH, Jang JS, Lee JH, Choi SR, Park BH. A comparison of the BISAP score and serum procalcitonin for predicting the severity of acute pancreatitis. Korean J Intern Med. 2013;28:322-9. [CrossRef] [PubMed]
28. Chen L, Lu G, Zhou Q, Zhan Q. Evaluation of the BISAP score in predicting severity and prognoses of acute pancreatitis in Chinese patients. Int Surg. 2013;98(1):6-12. [CrossRef] [PubMed]
29. Simchuk EJ, Traverso LW, Nukui Y, Kozarek RA. Computed tomography severity index is a predictor of outcomes for severe pancreatitis. Am J Surg. 2000;179:352-5. [CrossRef] [PubMed]
30. Leung TK, Lee CM, Lin SY, Chen HC, Wang HJ, Shen LK, Chen YY. Balthazar computed tomography severity index is superior to Ranson criteria and APACHE II scoring system in predicting acute pancreatitis outcome. World J Gastroenterol. 2005;11:6049-52. [PubMed]
31. Shinzeki M, Ueda T, Takeyama Y, Yasuda T, Matsumura N, Sawa H, Nakajima T, Matsumoto I, Fujita T, Ajiki T, Fujino Y, Kuroda Y. Predictors of early death in severe acute pancreatitis. J Gastroenterol. 2008;43:152-8. [CrossRef] [PubMed]
32. Lankisch PG, Pflichthofer D, Lehnick D. No strict correlation between necrosis and organ failyre in acute pancreatitis. Pancreas. 2000;20:319-22. [CrossRef] [PubMed]
33. Yang XN, Guo J, Lin ZQ, Huang L, Jin T, Wu W, Wen L, Zhang ZD, Xia Q, Hu WM. The study on causes of death in fulminant pancreatitis at early stage and late stage. Sichuan Da Xue Xue Bao Yi Xue Ban. 2011;42(5):686-90. [PubMed]

Reference as: Maheshwari N, Kumar A, Iqbal ZA, Mandal AK, Vyas A, Wig JD. Organ failure in acute pancreatitis and its impact on outcome in critical care. Southwest J Pulm Crit Care. 2015;10(5):253-64. doi: http://dx.doi.org/10.13175/swjpcc055-15 PDF

Ultrasound for Critical Care Physicians: Tiny Bubbles

Kashif Aslam, MD

Michel Boivin, MD

Division of Pulmonary, Critical care and Sleep Medicine

University of New Mexico School of Medicine

Albuquerque, NM

A 59 year old woman with a past medical history significant for stage IV MALT lymphoma (after chemotherapy and in remission) presented from a long term care facility for respiratory distress and altered mental status. The patient was in hypercarbic respiratory failure with a severe lactic acidosis. Her blood pressure deteriorated, she was begun on vasopressors and intubated.  Pertinent labs demonstrated a white blood cell count of 0.9 X10⁶ /ml, a hemoglobin of 7.1 g/dl, and a platelet count 66 X10⁶  /ml. The patient was started on Cefepime and Linezolid presumptively for septic shock. Ultrasounds of her thorax were performed (Videos 1 & 2).

Video 1.  Ultrasound of the right thorax in the mid-axillary line. 

 

Video 2.  Ultrasound of the right thorax in the mid-axillary line (slightly more caudad).

What is the best explanation for the ultrasound findings shown above? (Click on the correct answer for an explanation)

1. Large pleural effusion
2. Pneumothorax
3. Consolidation due to pneumonia
4. Ruptured diaphragm
5. Lung abscess

Reference as: Aslam K, Boivin M. Ultrasound for critical care physicians: tiny bubbles. Southwest J Pulm Crit Care. 2015;10(5):216-9. doi: http://dx.doi.org/10.13175/swjpcc067-15 PDF

May 2015 Critical Care Case of the Month: An Infected Leg

Sandra L. Till DO and Robert A. Raschke MD

Banner University Good Samaritan Medical Center

Phoenix, AZ

History of Present Illness

A 46-year-old transferred due to concern for necrotizing fasciitis. One the day prior to transfer purple discoloration was not noted in the lower portion of the left leg. On the day of transfer the leg became more purple, painful, and swollen. She presented to a pain clinic that advised her to go to an emergency room. The emergency room performed arterial Doppler ultrasound, which was normal and transferred her due to concern of necrotizing fasciitis.

Past Medical History, Social History and Family History

She has a past medical history of fibromyalgia. She had an extensive surgical history including an appendectomy, bladder implant, cholecystectomy, dilatation and curettage, esophageal repair, left femoral artery repair due to a motor vehicle accident, partial hysterectomy, left knee surgery, and several left leg operations with grafting. Family history was non-contributory. The patient was single with two children, and smoked 1-2 packs of cigarettes per day for 30 years. She denied any illicit drugs or alcohol abuse.

Medications

• Zolpidem
• Warfarin
• Furosemide
• Potassium Chloride
• Morphine sulfate
• Gabapentin
• Oxycodone
• Alprazolam
• Ondansetron
• Amitriptyline

Physical Examination

Vitals signs: Blood pressure 128/85 mm Hg, pulse 86 beat/min, respiratory rate 12, temperature 36.7º C, SPO2 96% on 2L/min of oxygen.

General: Non-toxic, alert and oriented x3, tearful due to pain.

The remainder of the physical examination was unremarkable except for the left lower extremity (Figure 1).

Figure 1. Photograph of the patient's left leg.

Which of the following are appropriate at this time? (Click on the correct answer to proceed to the second of five panels)

1. Blood cultures
2. Complete blood count, c-reactive protein, sodium, creatinine and glucose
3. Surgery consult
4. Wound culture
5. All of the above

Reference as: Till SL, Raschke RA. May 2015 critical care case of the month: an infected leg. Southwest J Pulm Crit Care. 2015;10(5):208-15. doi: http://dx.doi.org/10.13175/swjpcc045-15 PDF

April 2015 Critical Care Case of the Month: Half-Sided Light House

Theodore Loftsgard APRN, ACNP, CCRN

Adam Frost RRT, CRT

Dacia Evans RN

Karen Kolbet PharmD, RPh

Division of Critical Care

Mayo Clinic

Rochester, Minnesota

History of Present Illness

A 55 year old woman was transferred to the ICU from the general medicine ward for tachycardia and acute hypoxic respiratory distress. She has multiple myeloma and had received cycle one of bortezomib, dexamethasone, thalidomide, cisplatin, doxorubicin, cyclophosphamide and etoposide (VDT-PACE) and radiotherapy to T7 for a pathologic compression. She was admitted for pain control from mucositis.

Past Medical History

In addition to the multiple myeloma she has a past medical history of asthma, ovarian cysts, diverticulitis, eczema, pneumonia, laparoscopic cholecystectomy, total abdominal hysterectomy with bilateral salpingo-oophorectomy, appendectomy, ectopic pregnancy in the past, and left Bell's palsy.

Current Medications

• Acyclovir 400 mg BID
• Albuterol 90 HFA prn
• Allopurinol 300 mg daily
• Fluconazole 200 mg BID
• Gabapentin 300 mg BID,
• Hydromorphone
• Levofloxacin 500 daily
• Morphine
• Omeprazole
• Bactrim 400-80 mg daily for PCP prophylaxis
• Thalomid 200 mg capsule daily
• Ativan 0.5 mg just prior to transfer

Physical Examination

• Vital Signs: temperature 36.4 °C, respiratory rate 24 breaths/minute, blood pressure 148/77 mm Hg, pulse 133/minute, SpO2 98% on oxygen at 4 L/min.
• General: Alert and follows commands. Slightly somnolent. In respiratory acute distress.
• Skin: Pink, warm and dry without acute rashes or lesions.
• Eyes: EOMs intact. Conjunctivae pink. Sclerae anicteric
• ENT: Neck supple. Trachea midline.
• Cardiac: S1, S2 irregular rate and rhythm without extra sounds, murmurs, rubs or gallops. Capillary refill 2 seconds.
• Lungs: Respirations with accessory muscle use, shallow. scattered crackles and equal to auscultation. Diminished bilateral bases.
• Abdomen: Soft. No abdominal tenderness. Non-distended. Bowel sounds present.
• Extremities: Peripheral pulses +2/4 throughout. 1+ peripheral edema.
• Neuro: GCS = 13, residual bell's palsy.

Pertinent Labs

• Sodium: 144 mmol/L
• Potassium: 4.2 mmol/L
• Chloride: 113 mmol/L *
• Bicarbonate,: 23 mmol/L
• Creatinine: 0.6 mg/dL
• Hematocrit: 20.5 %
• Leukocytes: 0.5 x10(9)/L
• Hemoglobin: 6.2 g/dL
• Platelet Count: 39 x10(9)/L
• Calcium, Ionized(S): 4.81 mg/dL
• pH (FOR CALCIUM, IONIZED [S]): 7.47
• INR: 1.5
• APTT(P): 29 sec

Her ECG (Figure 1) showed a tachycardia with a maximum heart rate was in the 170's.

Figure 1. Admission ECG to the ICU.

Her admission chest x-ray is shown in Figure 2.

Figure 2. Portable chest x-ray taken just after admission to the ICU.

Which of the following are true? (Click on the correct answer to proceed to the second of four panels)

1. The EKG shows atrial fibrillation with a rapid ventricular response
2. She should be immediately intubated for airway protection
3. The chest x-ray shows bilateral pleural effusions
4. 1 and 3
5. All of the above

Reference as: Loftsgard T, Frost A, Evans D, Kolbet K. April 2015 critical care case of the month: half-sided light house. Southwest J Pulm Crit Care. 2015;10(4):159-70. doi: http://dx.doi.org/10.13175/swjpcc031-15 PDF

March 2015 Critical Care Case of the Month: It’s Not Always Sepsis

Dionne Morgan, MD 

Carolyn H. Welsh, MD 

University of Colorado and the Eastern Colorado Veterans Affairs Medical Center

Department of Medicine

Division of Pulmonary Sciences and Critical Care Medicine

Denver, CO

History of Present Illness

A 57-year-old man with multiple co-morbidities including diabetes mellitus presented with wet gangrene of the right foot and hypotension.  He had diabetic ketoacidosis and acute kidney injury. He was admitted to the medical intensive care unit, given intravenous fluids and treated with insulin therapy, piperacillin/tazobactam and vancomycin. Initial blood cultures grew Methicillin-resistant Staphylococcus aureus (MRSA). The podiatry service performed a right transmetatarsal amputation. Subsequently, he did well and was transferred to a medical floor for further care. 

Three weeks later, following resolution of the initial sepsis, he developed persistently high fevers with hemodynamic instability despite continued antibiotic therapy. He was transferred back to the MICU for presumed sepsis.

Past Medical History, Social History and Family History

The past medical history was significant for diabetes, hypertension, COPD, coronary artery disease and hepatitis C. He did not smoke nor drink alcohol. Family history was non-contributory.

Physical Examination

On readmission to the medical intensive care unit, the patient was noted to have a generalized maculopapular rash on both upper and lower extremities, torso, palms and soles of his feet, associated with facial and periorbital edema (Figure 1). There was no mucosal membrane involvement or lymphadenopathy.  He was also febrile to 104^o F, hypotensive to 80/50 mm Hg and icteric.

Figure 1. Image of rash.

Laboratory Studies

Initial labs showed elevated leukocyte count, BUN and creatinine with anion-gap metabolic acidosis but a normal liver enzyme profile. Repeat labs on readmission to the medical ICU were significant for severe leukocytosis, with marked eosinophilia, atypical lymphocytes on blood smear, acute transaminitis and hyperbilirubinemia.

Admission labs: White blood cell count (WBC) 29.9 x 1000 cells/μL. Eosinophils 0.0% (Normal 0.0 - 0.7%), AST 28 U/L, ALT 15 U/L, ALP 162 U/L, total bilirubin 0.2 mg/dL.

Labs on ICU readmission: White blood cell count (WBC) 35.7 x 1000 cells/ μL. Eosinophils 2.3% (Normal 0.0 -0.7%), AST 486 U/L, ALT 288 U/L, ALP 749 U/L, total bilirubin 4.3 mg/dL.

Which are components of the SIRS criteria? (click on the correct answer to proceed to the second of 4 panels)

1. Elevated respiratory rate
2. Hypothermia
3. Leukocytosis
4. Tachycardia
5. All the above

Reference as: Morgan D, Welsh CH. March 2015 critical care case of the month: it's not always sepsis. Southwest J Pulm Crit Care. 2015;10(3):105-11. doi: http://dx.doi.org/10.13175/swjpcc029-15 PDF

Ultrasound for Critical Care Physicians: Now My Heart Is Even More Full

Bilal Jalil, MD

Michel Boivin, MD

Division of Pulmonary, Critical Care and Sleep Medicine

University of New Mexico School of Medicine

Albuquerque, NM

A 49-year-old man with type 2 diabetes, intravenous drug abuse and heart failure presented to the emergency room with 2 weeks of progressively worsening chest pain, lower extremity swelling and shortness of breath. The patient was found to have an elevated troponin as well as brain natriuretic peptide and the absence of ischemic electrocardiogram findings. The patient was admitted to the medical ICU for hypoxic respiratory failure and shock of uncertain etiology. Clinically he seemed to be in decompensated heart failure and a bedside echocardiogram was performed (Figures 1 and 2).

Figure 1. Parasternal short axis view at the level of the aortic valve

Figure 2. Apical 4 chamber view.

What is the best explanation for the echocardiographic findings shown above? (Click on the correct answer for the explanation)

1. Atrial myxoma
2. Cardiac amyloidosis
3. Cardiac lymphoma
4. Takotsubo cardiomyopathy
5. Tricuspid valve endocarditis

Reference as: Jalil B, Boivin M. Ultrasound for critical care physicians: now my heart is even more full. Souhtwest J Pulm Crit Care. 2015;10(2):83-6. doi: http://dx.doi.org/10.13175/swjpcc020-15 PDF

February 2015 Critical Care Case of the Month: A Bloody Mess

Mily Sheth, MD

Carmen Luraschi, MD

Matthew P. Schreiber, MD, MHS

University of Nevada School of Medicine: Las Vegas

Department of Internal Medicine

Division of Pulmonary/Critical Care

Las Vegas, NV

History of Presenting Illness:

A 23-year-old Ethiopian woman with a known history of systemic lupus erythematosus (SLE) but of unknown duration presented with the chief complains of cough and generalised weakness for 1 week. She had a recent history of travelling to Ethiopia 3 months ago for 3 weeks. She complained of subjective fevers and one episode of blood tinged sputum. She also complained of fatigue and an episode of syncope which prompted her hospitalization.

PMH, SH and FH:

The patient has a past medical history of SLE diagnosed in Ethiopia of which no records were available. She is a student and denied alcohol, smoking or drug abuse. She denied any family history of autoimmune disorders. She did not take any medications at home.

Physical Examination:

Initial admission vital signs were temperature of 100.5 F, heart rate of 130, respiratory rate of 30 and blood pressure of 92/48. Oxygen saturation was 96% on 2 L/min via nasal cannula.

She appeared to be in moderate distress but was speaking in full sentences. Skin examination revealed a malar rash on her face. Her upper and lower extremities had excoriated plaques. Her anterior chest had flat non blanchable, macular rash. CVS examination revealed tachycardia without any murmurs. Respiratory exam was positive for bilaterally diffuse bronchial breath sounds. The remainder of her exam was within normal limits.

Laboratory and Radiology:

CBC: WBC 6.7 million cells/mcL, hemoglobin 7.1 g/dL, hematocrit 20.9, platelet 160,000 cells/mcL

Renal panel: within normal limits.

Troponin 0.01, creatine kinase 457 U/L, lactic acid 1.1 mm/L, HIV non-reactive

Liver function tests: AST 288 U/L, ALT 93 U/L alkaline phosphatase 136 IU/L, total bilirubin 0.9 mg/dL

Radiography:

Her initial chest x-ray is shown in figure 1. It was interpreted as showing diffuse pulmonary infiltrates, right lung greater than left. No pleural effusions. No pneumothorax.

Figure 1. Initial chest x-ray.

In a patient with these characteristics, which other test(s) would you order? (Click on the correct answer to proceed to the second of five panels)

1. Arterial blood gases and lactic acid
2. Cardiac angiogram
3. Computed tomography (CT) of the chest without contrast
4. VATS lung biopsy
5. All of the above

Reference as: Sheth M, Luraschi C, Schreiber MP. February 2015 critical care case of the month: a blood mess. Southwest J Pulm Crit Care. 2015;10(2):63-9. doi: http://dx.doi.org/10.13175/swjpcc148-14 PDF