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Southwest Pulmonary and Critical Care Fellowships

Critical Care

Last 50 Critical Care Postings

(Most recent listed first. Click on title to be directed to the manuscript.)

October 2024 Critical Care Case of the Month: Respiratory Failure in a
   Patient with Ulcerative Colitis
July 2024 Critical Care Case of the Month: Community-Acquired
   Meningitis
April 2024 Critical Care Case of the Month: A 53-year-old Man Presenting
   with Fatal Acute Intracranial Hemorrhage and Cryptogenic Disseminated
   Intravascular Coagulopathy
Delineating Gastrointestinal Dysfunction Variants in Severe Burn Injury
   Cases: A Retrospective Case Series with Literature Review
Doggonit! A Classic Case of Severe Capnocytophaga canimorsus Sepsis
January 2024 Critical Care Case of the Month: I See Tacoma
October 2023 Critical Care Case of the Month: Multi-Drug Resistant
   K. pneumoniae
May 2023 Critical Care Case of the Month: Not a Humerus Case
Essentials of Airway Management: The Best Tools and Positioning for 
   First-Attempt Intubation Success (Review)
March 2023 Critical Care Case of the Month: A Bad Egg
The Effect of Low Dose Dexamethasone on the Reduction of Hypoxaemia
   and Fat Embolism Syndrome After Long Bone Fractures
Unintended Consequence of Jesse’s Law in Arizona Critical Care Medicine
Impact of Cytomegalovirus DNAemia Below the Lower Limit of
   Quantification: Impact of Multistate Model in Lung Transplant Recipients
October 2022 Critical Care Case of the Month: A Middle-Aged Couple “Not
   Acting Right”
Point-of-Care Ultrasound and Right Ventricular Strain: Utility in the
   Diagnosis of Pulmonary Embolism
Point of Care Ultrasound Utility in the Setting of Chest Pain: A Case of
   Takotsubo Cardiomyopathy
A Case of Brugada Phenocopy in Adrenal Insufficiency-Related Pericarditis
Effect Of Exogenous Melatonin on the Incidence of Delirium and Its 
   Association with Severity of Illness in Postoperative Surgical ICU Patients
Pediculosis As a Possible Contributor to Community-Acquired MRSA
   Bacteremia and Native Mitral Valve Endocarditis
April 2022 Critical Care Case of the Month: Bullous Skin Lesions in
   the ICU
Leadership in Action: A Student-Run Designated Emphasis in
   Healthcare Leadership
MSSA Pericarditis in a Patient with Systemic Lupus
   Erythematosus Flare
January 2022 Critical Care Case of the Month: Ataque Isquémico
   Transitorio in Spanish 
Rapidly Fatal COVID-19-associated Acute Necrotizing
   Encephalopathy in a Previously Healthy 26-year-old Man 
Utility of Endobronchial Valves in a Patient with Bronchopleural Fistula in
   the Setting of COVID-19 Infection: A Case Report and Brief Review
October 2021 Critical Care Case of the Month: Unexpected Post-
   Operative Shock 
Impact of In Situ Education on Management of Cardiac Arrest after
   Cardiac Surgery
A Case and Brief Review of Bilious Ascites and Abdominal Compartment
   Syndrome from Pancreatitis-Induced Post-Roux-En-Y Gastric Remnant
   Leak
Methylene Blue Treatment of Pediatric Patients in the Cardiovascular
   Intensive Care Unit
July 2021 Critical Care Case of the Month: When a Chronic Disease
   Becomes Acute
Arizona Hospitals and Health Systems’ Statewide Collaboration Producing a 
   Triage Protocol During the COVID-19 Pandemic
Ultrasound for Critical Care Physicians: Sometimes It’s Better to Be Lucky
   than Smart
High Volume Plasma Exchange in Acute Liver Failure: A Brief Review
April 2021 Critical Care Case of the Month: Abnormal Acid-Base Balance
   in a Post-Partum Woman
First-Attempt Endotracheal Intubation Success Rate Using A Telescoping
   Steel Bougie 
January 2021 Critical Care Case of the Month: A 35-Year-Old Man Found
   Down on the Street
A Case of Athabaskan Brainstem Dysgenesis Syndrome and RSV
   Respiratory Failure
October 2020 Critical Care Case of the Month: Unexplained
   Encephalopathy Following Elective Plastic Surgery
Acute Type A Aortic Dissection in a Young Weightlifter: A Case Study with
   an In-Depth Literature Review
July 2020 Critical Care Case of the Month: Not the Pearl You Were
   Looking For...
Choosing Among Unproven Therapies for the Treatment of Life-Threatening
   COVID-19 Infection: A Clinician’s Opinion from the Bedside
April 2020 Critical Care Case of the Month: Another Emerging Cause
   for Infiltrative Lung Abnormalities
Further COVID-19 Infection Control and Management Recommendations for
   the ICU
COVID-19 Prevention and Control Recommendations for the ICU
Loperamide Abuse: A Case Report and Brief Review
Single-Use Telescopic Bougie: Case Series
Safety and Efficacy of Lung Recruitment Maneuvers in Pediatric Post-
   Operative Cardiac Patients
January 2020 Critical Care Case of the Month: A Code Post Lung 
   Needle Biopsy
October 2019 Critical Care Case of the Month: Running Naked in the
   Park

 

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.

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Tuesday
Oct012024

October 2024 Critical Care Case of the Month: Respiratory Failure in a Patient with Ulcerative Colitis

Lewis J. Wesselius MD

Pulmonary Department

Mayo Clinic Arizona

Scottsdale, AZ USA

History of Present Illness

The patient is a 57-year-old woman with a history of ulcerative colitis (UC) complicated by toxic megacolon with subsequent colectomy. She presented to the emergency department with cough, shortness of breath and hypoxemia (87% on RA).

PMH, SH

  • UC with history of toxic megacolon (4 years prior) with a total colectomy.
  • History of a prior episode of respiratory failure a year earlier thought possibly medication-induced (ustekinumab, Stelara®) which she was taking for her UC. She was treated with steroids with a good response.
  • Pyoderma gangrenosum of both ankles (attributed to UC).
  • Anemia of chronic disease.
  • She is a lifelong non-smoker.
  • No exposures to toxic dusts, birds, down, humidifiers, mold or other antigens associated with hypersensitivity pneumonitis.

Physical Exam

  • Afebrile, Oxygen saturation 94% on 2 lpm supplemental oxygen.
  • Chest: crackles noted at left base.
  • CV regular rhythm, no murmur.
  • Ext: scarring and erythema on both ankles consistent with resolving pyoderma gangrenosum.

Current Medications

  • Clonazepam 1.0 mg daily at bedtime
  • Gabapentin 300 mg TID
  • Pantoprazole 40 mg BID
  • Prednisone 5 mg daily

Laboratory

  • Hgb 9.7, WBC 16.9
  • Swabs for Influenza A/B and Covid were negative
  • Cocci serology negative

A chest radiograph was performed (Figure 1).

Figure 1. Portable chest X-ray performed in the emergency department. (To view Figure 1 in a separate, enlarged window click here).

Which of the following is/are true regarding the chest X-ray?

  1. There is a left lower lobe consolidation.
  2. The portable chest X-ray may be normal.
  3. A chest CT scan is required to definitely view any consolidation.
  4. There is a right upper lobe consolidation.
  5. All of the above.
Cite as: Wesselius LJ. October 2024 Critical Care Case of the Month: Respiratory Failure in a Patient with Ulcerative Colitis. Southwest J Pulm Crit Care Sleep. 2024;29(4):30-33. doi: https://doi.org/10.13175/swjpcc2046-24 PDF
Monday
Jul012024

July 2024 Critical Care Case of the Month: Community-Acquired Meningitis

Robert A. Raschke MD

The University of Arizona College of Medicine – Phoenix

Phoenix, AZ USA

History of Present Illness

A 59-year-old man was brought to our emergency department at 0300 with a possible stroke. He was last known well at 2230 the previous evening, when he complained of severe headache and took some acetaminophen before going to bed. His wife (who provided all history) noted that the patient awoke about midnight, vomited and took some naproxen. The wife next heard the patient awake at 0230, and found him back in the bathroom vomiting again, slow to respond, “mumbling” and confused. The wife was able to get the patient into their car with some difficulty and drove him to the ER.

Past Medical History, Social History, Family History

Only minimal past medical history was elicited. There was no known trauma, no fever and no recent illnesses. The patient took no prescription medications. He did not have any history of neurological disease or of substance abuse.

Physical Examination

Vitals from the ER at 0300 included: BP 157/130 mmHg, HR 101 bpm, RR 16 bpm, temperature 97.7°F.

The patient was described as “non-toxic appearing.” His eyes were open, but he was mute and didn’t obey commands. His Glascow Coma Scale was E4, V1, M5. Formal strength testing wasn’t performed, but he was observed to spontaneously move his arms. No facial asymmetry was noted.

Hospital Course

A “Stroke alert” was called based on the clinical presentation. The laboratory evaluation was significant for: WBCC 14.9x109/L, hemoglobin 13.2 g/L, platelets 181x109/L; Na 135 mmol/L, K 4.0 mmol/L, Cl 100 mmol/L, CO2 23 mmol/L, BUN 14 mg/dL, creatinine 0.7 mg/dL, glucose 349 mg/dL and INR 1.0. A procalcitonin was elevated at 0.8 ng/mL. Urinalysis showed >500 mg/dL glucose, moderate leukocyte esterase, WBCC 19/hpf, and no bacteria. A urine drugs of abuse screen was negative. CT head, CTA head/neck and brain perfusion scans were all negative for acute abnormalities. A virtual stroke neurologist recommended against lytics and/or thrombectomy, due to the lack of radiographic evidence of a large vessel occlusion.

The patient was admitted to the family medicine service. Ceftriaxone 1gm was administered for a presumed urinary tract infection. His temperature was retaken at 0630, at which time it had risen to 102.7°F. At 0730 the patient became agitated, diaphoretic and his SpO2 fell to 79%. His BP was 223/139 mmHg, HR 115 bpm, and RR 53 bpm and he was emergently intubated and transferred to the ICU.

Which of the following is false regarding the clinical findings of community-acquired bacterial meningitis? (Click on the correct answer to be directed to the second of 5 pages)

  1. Fifty percent of patients present within 24 hours of symptom onset.
  2. The majority of patients have the classic triad of fever, stiff neck and altered mental status.
  3. Ninety-five percent of patients have at least two of four findings: (headache, fever, stiff neck and altered mental status).
  4. Patients may less commonly present with community-acquired hemiplegia, aphasia, seizure, and cranial nerve deficits.
  5. All are true.
Cite as: Raschke RA.  2024 Critical Care Case of the Month: Community-Acquired Meningitis. Southwest J Pulm Crit Care Sleep. 2024;29(1):1-5. doi: https://doi.org/10.13175/swjpccs027-24 PDF
Monday
Apr012024

April 2024 Critical Care Case of the Month: A 53-year-old Man Presenting with Fatal Acute Intracranial Hemorrhage and Cryptogenic Disseminated Intravascular Coagulopathy

Robert A. Raschke MD MS 1,2

Kim Josen MD2

Ethan Weisman BS3

1Department of  Medicine and Biomedical Informatics, University of Arizona College of Medicine-Phoenix, Phoenix AZ USA

2Pulmonary and Critical Care Medicine, HonorHealth Osborne, Scottsdale, AZ USA

3 The Honors College, Arizona State University, Tempe, Arizona, USA

History of Present Illness: A 53-year-old man was admitted for acute onset of left hemiparesis, left facial droop and dysarthria witnessed by his wife (a nurse) while they were watching TV that evening. She reported the patient had no previous history of coronary artery disease or cerebral vascular disease, prior to an admission occurring three weeks earlier. The patient presented at that time with acute, severe left-sided chest pain that began while he was doing some heavy yardwork. While being evaluated in the emergency department (ED), he developed left-sided facial numbness, hemiparesis and dysarthria. A CT scan of the brain was normal. Neurological symptoms resolved before lytic therapy could be administered. Troponins and EKG were normal. A D-dimer was >20 mg/L, but a CTA of the chest showed no pulmonary embolism and was otherwise unrevealing. The chest pain resolved without specific therapy. Subsequent CTA of the head and neck and a brain MRI were both normal. Other labs drawn during that two-day hospitalization, including a CBC, complete metabolic profile, INR and aPTT, were all essentially normal. The patient was diagnosed with transient ischemic attack, atypical chest pain and new onset hypertension, and discharged on 81 mg aspirin and 2.5 mg amlodipine daily.

The patient did well over the intervening three weeks except for poor control of his hypertension, with blood pressures measured at home as high as 178/105. On the morning before his current presentation, the patient coughed up blood. The patient’s wife examined his mouth and noted several “blood blisters” of his buccal mucosa which she attributed to his poorly fitting dentures. The patient was otherwise well until the onset of stroke symptoms at 2200, after which he  complained of diffuse headache. 

Past Medical History: The patient had no known allergies. He had a history of emphysema, GERD and hypercholesterolemia and was taking rosuvastatin, esomeprazole and inhaled fluticasone/umeclidinium/vilanterol in addition to amlodipine and aspirin. He had a remote history of major trauma resulting in asplenia. He didn’t smoke, vape, drink alcohol excessively or use drugs. He worked as a truck driver.

Physical Examination: Initial physical examination was significant for HR 117 bpm, RR 18 bpm, temp. 36.5°C, BP 169/99 mmHg. His Glascow Coma Scale (GCS) was 14 and he was dysarthric, with a rightward gaze preference and a dense L hemiplegia. Ecchymoses of his left knee and right shoulder were noted. A stat CT brain showed a 6x4x4cm intraparenchymal hematoma centered on the right basal ganglia, effacing the right lateral ventricle and causing 6mm of midline shift. It was confirmed that the patient had not taken any antithrombotic medications or clopidogrel. Admission labs demonstrated a WBCC 22.8 x103/uL, Hb 12.8 g/dL and platelet count of 64 x103/uL. An automated five-part differential (neutrophils, lymphocytes, monocytes, basophils, and eosinophils) was normal. The INR was 2.2 and aPTT 38 secs. Fibrinogen was 62 mg/dL and a D-dimer >20 ml/L. A complete metabolic profile was unremarkable.

Routine management of acute hemorrhagic stroke includes which of the following except? (Click on the correct answer to be directed to the )

  1. Rapid control of systolic blood pressure to levels <140mmHg using intravenous antihypertensives if necessary.
  2. Rapid reversal of antithrombotic effects of medications such as warfarin with four-factor prothrombin complex concentrate (4F PCC), and Xa inhibitors with andexanet alpha or 4FPCC.
  3. Platelet transfusion to maintain platelet count >100 x103/uL in patients with thrombocytopenia.
  4. Platelet transfusion to restore platelet function in patients with normal platelet counts, but platelet dysfunction due to aspirin or other antiplatelet drugs.
  5. Neurosurgical consultation.
Cite as: Raschke RA, Josen KM, Weisman E. A 53-year-old Man Presenting with Fatal Acute Intracranial Hemorrhage and Cryptogenic Disseminated Intravascular Coagulopathy. Southwest J Pulm Crit Care Sleep. 2024;28(4):49-55. doi: https://doi.org/10.13175/swjpccs016-24 PDF 
Wednesday
Mar202024

Delineating Gastrointestinal Dysfunction Variants in Severe Burn Injury Cases: A Retrospective Case Series with Literature Review

Sriharsha Rapaka MD 1,2

Priyankar Kumar Datta MD, DNB, DM 3

Shashikant Sharma MD, DM 3,4

1Intensive Care Medicine, St John of God Healthcare, Victoria, Australia

2Critical Care Medicine, All India Institute of Medical Sciences, New Delhi, India

3Anaesthesiology, Pain Medicine and Critical Care, All India Institute of Medical Sciences, New Delhi, India

4Critical Care Medicine, Jayaprabha Medanta Hospital, Patna, India

Abstract 

Background: Severe burns can significantly impact various organ systems, including the gastrointestinal (GI) system. GI complications are frequently observed in patients with over 20% total body surface area (TBSA) burn.

Objectives: This case series delves into the intricate phenomenology of post-burn GI dysfunction, challenging conventional cause-and-effect paradigms. Our aim is to discern, comprehend, and explore variables influencing positive and negative outcomes, laying the foundation for further research given the current heterogeneity in the literature.

Methods: Severe burn patients with GI dysfunction identified between April 1, 2022, and July 31, 2022, from the institutional database are included in this retrospective case-series, and comparisons were made across baseline and treatment conditions across participants. Data were collected on demographics, burn characteristics, complications, and treatment outcomes.

Results: We analysed 12 patients with severe burns and GI dysfunction and categorized them into two patterns: Pattern A, characterised by early onset symptoms, gastric and small bowel dilatation, and a relatively benign course with high recovery rates was observed in 6 patients; and Pattern B, characterised by late-onset symptoms, colonic dilatation, shock, and a high mortality rate due to megacolon was seen in 6 patients.

Conclusion: The post-burn GI dysfunction observed in our study is a complex interplay of multiple factors. Adequate fluid resuscitation, timely excision of necrotic tissue, staged food ingestion, specific nutrient administration, and appropriate use of antibiotics and judicious use of selective digestive decontamination (SDD) are essential strategies to prevent and treat this syndrome.

Introduction

Severe burns can have significant physiological impacts on the body, posing a risk to a patient's life that may be exacerbated by complications throughout the stages of treatment (1,2). Gastrointestinal (GI) complications are common in partial and full-thickness burns involving more than 20% TBSA and can include constipation, delayed gastric emptying, bacterial translocation, and sepsis, among others (2,3). While animal models suggest that burns delay gastric emptying and affect gut motility, the exact mechanism in humans is unknown (4,5). Probable causes could include large-volume fluid resuscitation, immobility, increased sympathetic drive secondary to pain, and dietary association with glutamine, opioids, and drugs such as tramadol and tapentadol. This study aims to describe two distinct patterns of bowel dysfunction observed in patients admitted with severe burns and discuss the impact of thermal injuries on gut motility and associated outcomes.

Methodology

Our study includes adult and paediatric patients with severe burns (>20% TBSA) and post-burn GI dysfunction, identified between April 1, 2022, and July 31, 2022. Data collection from discharge codes and chart reviews was conducted independently by two qualified, trained personnel for every participant from the medical records of eligible patients, employing anonymization protocols to uphold patient confidentiality during the entirety of the process. Data, including demographics, burn characteristics, complications, and response to treatment, were collected for the entire course of clinical care and subsequently compiled and reported. The burn unit at the hospital is staffed with highly skilled clinical staff members who have specialized training in treating severe burns. The assessment of treatments and data was supervised by an expert analyst at the faculty level. 

Case Descriptions

The long-term outcome of a burn injury dramatically depends on the quality of care received during the initial hours. However, the majority of initial burn care is administered outside of specialized burn centres. It is essential to comprehend the intricacies of Advanced Burn Life Support (ABLS) to ensure the patient's optimal outcome. The medical team provided comprehensive intensive care to manage the patients' GI dysfunction and a description of the management, and treatment approach is summarised below.

  1. Symptoms: Patients with severe burns presented with symptoms such as diarrhoea, constipation, feed intolerance, abdominal distension, and hypoactive or diminished bowel sounds.
  2. Workup for diarrhoea: Patients underwent a workup that included testing for C. difficile toxin and stool culture and sensitivity, which both came back negative.
  3. Treatment for diarrhoea: Patients were treated with oral rehydration solution (ORS), probiotics, and racecadotril capsule (1.5mg/kg). Osmotic diarrhoea mostly resolved with reducing feed volume and protein content. In non-responders with suspected C. difficile infection presenting with fever, leucocytosis and pain abdomen, stool sample for toxin detection or culture was sent and oral metronidazole and, or oral vancomycin therapy was initiated. In patients who progressed to paralytic ileus, IV metronidazole along with oral vancomycin and vancomycin enema were administered.
  4. Treatment for constipation: Patients received syrup lactulose or syrup sodium picosulfate, liquid paraffin and milk of magnesia. Additionally, prokinetic agents were administered, and if necessary, enemas were used.
  5. Management of abdominal distension: In cases of abdominal distension, bowel decompression was performed by inserting a nasogastric tube with an intermittent suction system. This procedure aimed to reduce or resolve gastric dilatation, prevent vomiting and decrease the risk of aspiration associated with paralytic ileus.
  6. Intra-abdominal pressure (IAP) monitoring: Patients with abdominal distension underwent regular IAP monitoring, typically every 4 hours using indirect measurement via the bladder. If IAP exceeded 12 mmHg and was accompanied by hypotension, decreased urine output, or a tense abdomen, more frequent measurements (every 2 hours) were performed. Foley's catheter was also checked for blockage in case of increased IAP values. Monitoring continued until IAP levels dropped below 10 mmHg for several hours, along with clinical improvement.
  7. Stress ulcer prophylaxis and thromboprophylaxis: Patients above the age of 3 received pantoprazole for stress ulcer prophylaxis. Additionally, adult patients received injection Enoxaparin (1mg/kg) for thromboprophylaxis and mechanical prophylaxis. These measures were continued until patients achieved full ambulation.
  8. Antibiotics: Antibiotics were initiated only when signs of infection were observed, based on clinical assessment and monitoring of laboratory trends. Once definitive evidence of microbial growth from blood, urine, and wound cultures was obtained, culture-based antibiotics were started.
  9. Source control: Whenever necessary, the surgical team performed source control procedures to address and manage the underlying cause.

Patient Characteristics

Patients were separated into two patterns based on their clinical characteristics and outcomes (Table 1) and abdominal X-rays (Table 2).

Table 1. Comparison of the Two Patterns of Presentation (to view Table 1 in a new and separate window click here)

  • AKI=acute kidney injury

Table 2. Abdominal X-ray Patterns (to view Table 2 in a new and separate window click here)

Additional patient characteristics of pattern A and B are shown tables 3 and 4.

Table 3. Clinical Characteristics, Laboratory, and Imaging Findings of Patients with Pattern A GI Dysfunction (to view Table 3 in a new and separate window click here)

  • TBSA=total burn surface area
  • SOFA=Sequential Organ Failure Assessment Score

Table 4. Clinical Characteristics, Laboratory, and Imaging Findings of Patients with Pattern B GI Dysfunction (to view Table 4 in a new and separate window click here)

The two groups differed in baseline characteristics. The first group had a smaller median TBSA compared to the second group (32.5% vs 42.5%). Additionally, the first group comprised primarily paediatric patients, and their GI dysfunction developed earlier (median day 3 vs day 10), with a lower median SOFA score (0 vs 1). The second group had colonic dilatation in addition to gastric and small bowel dilatation, and all patients had signs and, or evidence of infection and were on antibiotics by the time they developed GI dysfunction. The median serum potassium levels were also slightly different between the two groups (3.8 vs 4.2). Notably, there were more deaths in the second group (50%) compared to the first group, where most patients recovered and were shifted to a step-down unit.

Discussion

The stress response, metabolic changes, and nutritional deficiencies primarily cause most gastrointestinal (GI) issues associated with burn injuries. If not promptly recognized and appropriately treated, these complications can lead to severe consequences, including fatal haemorrhage or perforation. Implementing early prophylactic measures during the post-burn period is crucial to prevent these outcomes. One common complication of thermal injuries is gastric distention and dysfunction.

Studies have shown that gastric emptying is significantly reduced by approximately 37-42% at 6 hours after a burn (4-6). In our study, we observed early gastric dilation upon admission. Burn injuries also affect the standard slow wave frequency in the stomach, increasing the occurrence of bradygastria (7). However, patients who arrived at the emergency department within 2 hours of the burn injury and received timely resuscitation mostly remained asymptomatic. Radiological evidence revealed gastric dilation, which eventually resolved during their hospital stay.

Animal studies have demonstrated that small intestinal transit time is significantly decreased in burn injury models compared to control groups at 2 hours (8,9) and 6 hours post-burn (5,6,9,10). In our study, we observed early small bowel dilation and ileus during the ICU stay. Chen et al conducted a study with rat models, revealing that the gastrointestinal motility in burn-injured rats treated with saline is notably higher compared to untreated burn-injured rats (11). This finding aligns with our observations, as most patients who arrived early and received timely resuscitation showed resolution of bowel dilation.

Colonic transit time was delayed compared to the control group in burn injury patients (5,12).  We could not find any literature on this topic in human subjects, highlighting the need for prospective studies. We noticed colonic involvement in symptomatic patients approximately one week after the burn injury. In cases of severe abdominal distension, dilated bowel loops, and feed intolerance, supplemental parenteral nutrition/TPN was administered. Early fluid resuscitation within 2 hours of a thermal injury is crucial in preventing multiple organ failure and mortality (18).

As described above, "Pattern A" patients experienced early symptoms during their ICU stay, showed minimal signs of infection, and had a relatively milder course with a lower mortality rate compared to "Pattern B" patients. Pattern B patients presented later, experienced more complications, and had higher morbidity and mortality rates. Dysmotility in these patients could be attributed to sepsis, opioids, or antibiotics. We tested for C. difficile toxin and culture, which came back negative. Immobility, opioid use, pain, and dietary glutamine are common causes of GI dysfunction in both patient groups. Incremental fentanyl infusion was administered to all patients within 24-48 hours of the injury. Breakthrough and procedural pain were managed with sub-anaesthetic doses of IV ketamine and IV fentanyl. Patients presenting with Pattern B symptoms were often prescribed slow-release oral tramadol/oral tapentadol/ pregabalin formulations to supplement or replace opioids due to concerns about constipation, tolerance, and addiction. Opioids could exacerbate GI symptoms like vomiting and constipation (14). Tramadol was found to delay colonic transit but did not affect upper gastrointestinal transit.15 Tapentadol, on the other hand, provided analgesia with a more tolerable side effect profile and resulted in less deterioration of gastrointestinal function and symptoms compared to standard opioids (16,17). However, results from different studies on tapentadol’ s effects on gastric emptying and bowel function are inconsistent, making its routine use in severe burns unclear (18,19). NSAIDs are effective for mild to moderate burns, but opioids are preferred in severe cases due to acute kidney injury (AKI) concerns. AKI is common in severe burns and an independent mortality risk factor. While opioids and NSAIDs may have contributed to large bowel dysmotility in Pattern B patients, a causal relationship cannot be established.

Burn-injured patients often experience acute and chronic neuropathic pain. Pregabalin has shown efficacy in reducing neuropathic pain and improving sleep but may cause constipation (20,21). Stress ulcer prophylaxis with pantoprazole was administered to patients above three years of age. Short-term treatment with proton pump inhibitors (PPIs) has been reported to delay gastric emptying of solid meals in healthy individuals (22). The effects of PPIs on liquid emptying are inconsistent (23). Prolonged gastric residence of PPIs due to delayed emptying may impact their pharmacological effectiveness, which can be clinically relevant in managing conditions such as GERD, functional dyspepsia, and diabetes (24). However, routine administration of PPIs in severe burn patients is not recommended. Although a systematic review and meta-analysis suggested a potential correlation between the usage of proton pump inhibitors (PPIs) and a heightened likelihood of contracting Clostridium difficile infection (CDI), we did not find any substantiating evidence of CDI (25). Further high-quality and prospective studies are needed to establish a causal relationship.

Major burns trigger an inflammatory response and catabolism, which can lead to severe nutrition deficiencies when combined with burn wound nutrient losses. These deficiencies can impair immune function and wound healing and increase the risk of organ injury and mortality (26). Sepsis causes dysbiosis and bacterial translocation (27). Severe burn patients frequently experience sepsis-induced ileus (28). Early and staged enteral nutrition has been shown to reduce gram-negative bacteraemia in burn patients and promote a healthy intestinal microenvironment (29-32). Caloric requirements were calculated using the Curreri formula for adults and Curreri junior formula for paediatric patients. However, as the formula often overestimates caloric needs, a target of 70-80% of the calculated requirement was set. Using continuous feeding bags, oral and/or nasogastric feeding was initiated from day 1 in the ICU. Post-pyloric feeding was administered to patients with feed intolerance or high gastric residual volume. Micronutrients and trace elements were supplemented, and glutamine and fibre were added to the diet for adult patients. Glutamine stimulates the release of glucagon-like peptide-1, which increases postprandial insulin secretion and slows gastric emptying (33). Current recommendations support using glutamine in severe burn patients due to promising evidence and minimal adverse effects. The RE-ENERGIZE trial showed mortality at 6 months was 17.2% in the glutamine group and 16.2% in the placebo group (hazard ratio for death, 1.06; 95% CI, 0.80 to 1.41) and no substantial between-group differences in serious adverse events (26).

We hypothesize that prudent utilization of selective digestive decontamination (SDD) may reduce infections and improve survival in severe burn patients (34). In a randomized trial, SDD demonstrated improved survival. However, according to a meta-analysis, enteral antibiotic use did not reduce mortality in severe burn patients, which aligns with our findings (35).

Managing wounds in the early stages and providing postoperative care after skin grafting pose challenges in patients with extensive burns. Effective use of negative pressure wound therapy (NPWT) can facilitate better wound healing and reduce infections. Patients with burns involving the perineum and genitalia present particular challenges due to increased wound infections, graft loss, and sepsis caused by dressing soiling (36-38). We hypothesize that faecal management systems might reduce infections by diverting faeces and improving personal hygiene in severe burn patients. A retrospective study found a survival benefit with no significant complications associated with faecal management systems (39).

Limitations

Our study is a retrospective case series that has inherent constraints. Our study lacked a control group. Selection bias and treatment assignment bias cannot be ruled out. These unregulated and unidentified factors of variation have the potential to influence the general applicability of the study's outcomes. Further prospective studies are needed to establish causal associations.

Conclusions 

The first pattern of patients, primarily children without underlying health conditions, appeared to have experienced bowel dysfunction as a stress response amplified using PPIs. Diarrhoea in these cases was not due to an infection, and excessive sympathetic activity could be the contributing factor. On the other hand, the second pattern of patients, primarily adults with comorbidities, were seriously ill and received a combination of antibiotics, opioids, and gabapentin. These patients were also experiencing sepsis and sepsis-induced ileus, which is common in individuals with severe burns. In this group, diarrhoea could be caused by an infectious or non-infectious agent, and while testing for C. difficile was negative, there may have been delays in the transportation and analysis of stool samples that resulted in false negative results. It is important to note that repeating the tests is unlikely to improve the sensitivity of the results (40).Top of Form

Learning Points

  1. Post-burn gastrointestinal issues are caused by a combination of factors that disrupt the balance of gut microbes leading to sepsis and multiple organ dysfunction syndrome (MODS).
  2. Further prospective studies are needed to establish the effect of tramadol, tapentadol and pregabalin on GI system in severe burns.
  3. The regular use of PPIs may worsen the impact of severe burns on the gut.
  4. Managing serious burns necessitates a collaborative strategy encompassing prompt and effective fluid replacement, timely removal of deceased tissue, cautious initiation of nutrition, targeted use of antibiotics, and thoughtful application of selective digestive decontamination (SDD) to prevent gastrointestinal complications and reduce mortality.
  5. Faecal management systems and negative pressure wound therapy (NPWT) can help to improve wound care and hygiene in patients with perineal burns.

References

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Cite as: Rapaka S, Datta PK, Sharma S. Delineating Gastrointestinal Dysfunction Variants in Severe Burn Injury Cases: A Retrospective Case Series with Literature Review. Southwest J Pulm Crit Care Sleep. 2024;28(3):40-48. doi: https://doi.org/10.13175/swjpccs006-24 PDF 
Friday
Mar152024

Doggonit! A Classic Case of Severe Capnocytophaga canimorsus Sepsis

Brittany Denzer MD1

Minh Do MD1

Alexandra N. Fuher MD1

Logan Harper MD2

Kaleigh Lindholm MD3

Kara Calhoun MD MPH4

Kara Mould MD MPH4,5

1Department of Internal Medicine, University of Colorado Anschutz Medical Campus (Aurora) (Denzer, Do, Fuher)

2Department of Family Medicine, University of Colorado Anschutz Medical Campus (Aurora) (Harper)

3Department of Pathology, Denver Health (Denver) (Lindholm)

4Department of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus (Aurora) (Calhoun, Mould)

5Department of Medicine, Division of Pulmonary, Critical Care & Sleep Medicine, National Jewish Health (Denver) (Mould)

Abstract

Capnocytophaga canimorsus is a commensal organism often found in the oropharyngeal tracts of dogs and cats, capable of causing significant morbidity and mortality in immunocompromised patients. Early identification of C. canimorsus is challenging due to the organism’s rare presentation, rapid clinical progression, and slow growth on microbiological media. We present a case of a 47-year-old man with exposure to snakes and dogs, and history of severe alcohol use disorder, who presented to the emergency department with acute generalized abdominal pain. His course was notable for progressive respiratory failure requiring intubation and multi-pressor septic shock with minimal response to initial broad-spectrum antibiotics, complicated by hypoglycemia and DIC with purpura fulminans. Multidisciplinary review of the peripheral smear, notable for long, thin, intra and extracellular gram-negative rods, rapidly characterized our pathogen as an atypical gram-negative rod. With additional review of medical history and zoonotic exposures, we were able to quickly identify and address our concern for C. canimorsus, broadening our antibiotics to account for resistance patterns particular to this organism.

Case Presentation

A 47-year-old man with severe alcohol use disorder and exposure to pet dogs and snakes presented to the emergency department with one day of generalized abdominal pain. He was normotensive, febrile (39.5°C), tachycardic (151 beats/minute), and in respiratory distress with tachypnea (44 breaths/minute) and hypoxia (70% SpO2 on room air). His exam was notable for bibasilar rales and a diffusely tender abdomen with rigidity and guarding. There was an inch-long superficial laceration on the patient’s left anterior thigh. Labs were notable for WBC 4.1k/uL, hemoglobin 14.9g/dL, platelets 33k/uL, glucose 36mg/dL, lactate 10.8mmol/L, AST 115U/L, ALT 48U/L, alkaline phosphatase 111U/L, PT 27.4 seconds, PTT 136 seconds, D-dimer >20ug/mL, and fibrinogen 151mg/dL. Chest radiograph demonstrated bibasilar airspace opacities. CT abdomen and pelvis showed gallbladder wall thickening and edema without gallstones. A peripheral blood smear showed long, thin, intra and extracellular gram-negative rods (Figure 1).

Figure 1. Peripheral blood smear with findings of long, thin, intra- and extracellular gram-negative rods, identified with arrows. To view Figure 1 in a separate, enlarged window click here.

Hospital Course

Metronidazole and levofloxacin were started in the emergency department for gram-negative sepsis with concern for gastrointestinal source. A dextrose infusion was started for hypoglycemia and hematology was consulted for disseminated intravascular coagulation (DIC). The patient developed rapid respiratory failure requiring intubation, so antibiotics were broadened with the addition of vancomycin and cefepime, and the patient was admitted to the medical intensive care unit. Subsequently, blood culture multiplex PCR returned negative for common organisms, including Salmonella, initially of concern due to his recent snake exposure.  On day two, he developed multipressor shock and a purpuric rash involving his extremities (Figure 2).

Figure 2. Purpuric skin findings involving bilateral upper and lower extremities. To view Figure 2 in a separate, enlarged window click here.

Further history revealed the scratch on his thigh was from a dog. A multidisciplinary review of the case involving pathology, infectious disease, and intensive care teams identified Capnocytophaga canimorsus as an organism of concern given its consistence with the peripheral smear organism, as well as the clinical presentation of shock, DIC, and purpura fulminans in a patient with a dog scratch and alcohol use disorder. Antibiotics were changed to imipenem and levofloxacin with rapid improvement over the next several hours, weaning of vasopressors, and extubation. Antibiotics were further narrowed to ertapenem, then ampicillin-sulbactam after a penicillin allergy was deemed low risk. After twelve days of growth, blood cultures grew anaerobic gram-negative bacilli consistent with Capnocytophaga canimorsus.

Discussion

C. canimorsus is a bacteria found in the oropharyngeal tracts of dogs and cats; transmission is often associated with bites, scratches, or close contact with infected hosts, though there are also cases without documented animal contact (1). C. canimorsus causes significant disease in immunosuppressed patients and with asplenia or chronic heavy alcohol use (1,2). C. canimorsus infections carry a high mortality rate, estimated as high as fifty-five percent in septic patients (3,4). Unfortunately, identification of C. canimorsus is challenging and frequently delayed due to the organism's rare presentation and slow growth on microbiological media.

This case highlights a classic presentation of severe C. canimorsus infection including shock, hypoglycemia, DIC with purpura fulminans in a patient with heavy alcohol use and a recent dog scratch. In addition to early recognition of these typical features, multidisciplinary review of peripheral smear was essential to early suspicion for C. canimorsus.

DIC is seen in approximately 13% of C. canimorsus cases and is associated with high mortality (2,5). Purpura fulminans is a rare manifestation of DIC characterized by microvascular thrombosis leading to skin necrosis (5). Complications of purpura fulminans include gangrene, often requiring amputation, which was later seen with our patient, and contributes to significant disability.

C. canimorsus is often treated initially with broad spectrum antibiotics given its fastidious growth (3). Our patient declined despite escalating spectrum of antibiotics including levofloxacin, metronidazole, vancomycin, and cefepime, but rapidly improved following change to imipenem and levofloxacin, which was further narrowed to ertapenem, then ampicillin-sulbactam. This may be explained by resistant beta-lactamase producing strains of Capnocytophaga species, which are increasingly reported (3). Due to resistance, a carbapenem or beta-latamase inhibitor combination antibiotic is recommended (3). Early consideration of resistance patterns of C. canimorsus is essential in decreasing risk of complications associated with this organism (3,5).

Multidisciplinary review of the peripheral smear showing long, thin, intra- and extracellular gram-negative rods was essential for our early suspicion for C. canimorsus. With specific growth conditions and mean culture positivity of six days, traditional culture techniques making timely identification of C. canimorsus challenging. (2,4). In the case above, final identification by culture did not occur until the twelfth day of admission; notably, PCR testing is not standardly available and MALDI-TOF failed to provide earlier identification. Therefore, interdisciplinary review of the peripheral smear and recognition of classic clinical features of C. canimorsus infection proved critical in our rapid identification of the culprit organism.

Teaching Points:

  • Capnocytophaga canimorsus is a bacterium commonly found in dog mouths, capable of causing devastating disease in immunocompromised patients.
  • Severe presentations may include septic shock, hypoglycemia and DIC, and are associated with significant morbidity and mortality.
  • Early identification of C. canimorsus is often challenging due to the organism's rare presentation and slow growth on microbiological media. Peripheral smear may be of diagnostic value in bacteremic patients.
  • It is critical that providers maintain a high clinical suspicion for C. canimorsus in at-risk patients and treat them with antibiotics that consider possible resistance patterns.

References

  1. Chesdachai S, Tai DBG, Yetmar ZA, Misra A, Ough N, Abu Saleh O. The Characteristics of Capnocytophaga Infection: 10 Years of Experience. Open Forum Infect Dis. 2021 Apr 15;8(7):ofab175. [CrossRef][PubMed]
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  3. Killington K, Lee N, Asher R, Farrant O, Stone N. Purpura fulminans secondary to Capnocytophaga canimorsus bacteraemia following a dog bite: A case report and review of literature. Access Microbiol. 2023 Jun 16;5(6):acmi000505.v3. [CrossRef][PubMed]
  4. Zajkowska J, Król M, Falkowski D, Syed N, Kamieńska A. Capnocytophaga canimorsus – an underestimated danger after dog or cat bite – review of literature. Przegl Epidemiol. 2016;70(2):289-295. [PubMed]
  5. Perera TB, Murphy-Lavoie HM. Purpura Fulminans. 2023 Jul 17. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. [PubMed]
Cite as: Denzer B, Do M, Fuher AN, Harper L, Lindholm K, Calhoun K, Mould K. Doggonit! A Classic Case of Severe Capnocytophaga canimorsus Sepsis. Southwest J Pulm Crit Care Sleep. 2024;28(3):36-39. doi: https://doi.org/10.13175/swjpccs003-24 PDF