Cryptic Shock – Identifying the Unseen (PART 1)

Case Presentation

A 68-year-old man presented to the Emergency Department with complaints of breathing difficulty and fever for three days. The patient is a known diabetic and hypertensive.

After detailed history taking, clinical examination, and radiological workup, the patient was diagnosed with right-sided lobar pneumonia (Community-acquired) and immediately started on intravenous antibiotics. In addition, necessary cultures and blood samples were taken for evaluation.

At the time of presentation, his vitals were HR – 92/min, BP – 130/70mmHg, RR – 30/min, SpO2 – 90% with RA à 96% with 2L O2. He underwent bladder catheterization.

During the 1st hour in the ER, the patient had a very low urine output, which continued for the next few hours. Lactate levels were more than 4mmol/L.

Based on the symptoms, oliguria, and hyperlactatemia, the patient was diagnosed to have sepsis and was initiated on fluid resuscitation. After 2 hours, the patient remained oliguric still, and his BP declined to 120/70mmHg.

After 6 hours, the patient’s BP became 110/60mmHg (MAP – 77). He became anuric and developed altered sensorium. Since he did not meet the criteria of septic shock, he was continued on IV fluids and antibiotics.

After 12 hours, the BP became 80/40mmHg (MAP – 63mmHg) à developed Multiorgan Dysfunction Syndrome. He was then started on vasopressors and mechanical ventilation.

By day 3, the patient further deteriorated and went into cardiac arrest. ROSC was not achieved.

Case Analysis

The treatment initiated was based on protocols like Surviving Sepsis Guidelines and Septic Shock management. So how did the process fail in order to adequately resuscitate this patient? Could something have been done more differently?

The case you read above is a very common scenario. Approximately 30% of the people coming to the ER are hypertensive, and around 10% have diabetes mellitus. They form a huge population, among whom the incidence of any other disease increases their morbidity and early mortality.

Before we delve into the pathology in these patients, let us look at the basic definitions of shock/hypotension.

  • SBP < 90mmHg
  • MAP < 65 mmHg
  • Decrease in SBP > 40mmHg
  • Organ Dysfunction
  • Hyperlactatemia
  • Shock: A state of circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and demand (consumption), resulting in end-organ dysfunction.
  • Septic Shock: Adult patients can be identified using the clinical criteria of hypotension requiring the use of vasopressors to maintain MAP of 65mmHg or greater and having a serum lactate level greater than 2 mmol/L persisting after adequate fluids resuscitation.
  • Cryptic Shock: Presence of hyperlactatemia (or systemic hypoperfusion) in a case of sepsis with normotension.

Based on all the information given above;

  1. what do you think was wrong with our patient?
  2. What kind of shock did he have?
  3. Could we have managed him any other way?
  4. When should we have started inotropes?
  5. Did the fact that he was hypertensive and diabetic have to do with his early deterioration? If so, how?
  6. When did the patient-first develop signs of shock?
  7. What are the different signs and symptoms of shock, and how are they recognized in the ER?

Keep your answers ready… 

Part 2 of Cryptic Shock Series – Vascular Pathology and What is considered ‘Shock’ in Hypertensive patients

Part 3 of Cryptic Shock Series – Individualised BP management

Part 4 of Cryptic Shock Series – Latest Trends

References and Further Reading

  1. Ranzani OT, Monteiro MB, Ferreira EM, Santos SR, Machado FR, Noritomi DT; Grupo de Cuidados Críticos Amil. Reclassifying the spectrum of septic patients using lactate: severe sepsis, cryptic shock, vasoplegic shock and dysoxic shock. Rev Bras Ter Intensiva. 2013 Oct-Dec;25(4):270-8. doi: 10.5935/0103-507X.20130047.
  2. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):801-10. doi: 10.1001/jama.2016.0287.
  3. Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M; Sepsis Definitions Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):775-87. doi: 10.1001/jama.2016.0289.
  4. Education Resources – Sepsis Trust
  5. The Research of Predicting Septic Shock – International Emergency Medicine Education Project (iem-student.org)
  6. Sepsis – International Emergency Medicine Education Project (iem-student.org)
  7. Empiric Antibiotics for Sepsis in the ED Infographics – International Emergency Medicine Education Project (iem-student.org)
  8. Sepsis – An Overview and Update – International Emergency Medicine Education Project (iem-student.org)
Cite this article as: Gayatri Lekshmi Madhavan, India, "Cryptic Shock – Identifying the Unseen (PART 1)," in International Emergency Medicine Education Project, October 4, 2021, https://iem-student.org/2021/10/04/cryptic-shock/, date accessed: September 30, 2022

The Case of the Perplexing Crepitations

perplexing crepitations

Occam’s Razor – the simplest explanation is most likely to be correct.

In the Emergency Room, we are faced with a multitude of cases, and Occam’s Razor serves best when we need to narrow down on the differential diagnoses.

Sometimes, a few cases may evade this category and continue to baffle us even after a thorough history is obtained or a detailed clinical examination is performed. If we are lucky enough to get the point-of-care (POC) lab tests in time (or the mere availability of POC), they aid in the diagnosis and decision-making. At times, these POC lab tests also may not provide much help.

I have described one such case – a 21-year-old male with fever, dyspnea, desaturation, and multiple petechiae of 3 days duration.

Case Presentation

A 21-year-old male came at 9.30 pm to the ER with fever and breathlessness for three days. Being a healthcare worker himself, he had suspected pneumonia and started oral Amoxiclav, oral Clarithromycin, and Paracetamol. Despite this, there was no improvement in clinical status. He had progressively worsening breathlessness and continuous low-grade fever. On day 3, he developed a few petechial spots over his arms and minimal subconjunctival hemorrhage.

He recalls having myalgia in the lead up to these symptoms, for which he had received several injections of intramuscular Diclofenac. The injection sites now had developed small hematomas. There were no other visible bleeding manifestations. He clearly said that he had had no contact with any infectious patients and had self-isolated after developing these symptoms. His workplace had sent blood and sputum cultures – which came back negative. Their only concern was a continuous rise in the WBC count and sent to our hospital for further management.

Assessment

The patient was very ill-looking and extremely dyspneic with obvious usage of accessory respiratory muscles. He was profusely diaphoretic, had bilateral subconjunctival hemorrhage, multiple petechiae, anasarca, dyspnea, and 99.6⁰F. His Vitals were heart rate – 134/min, blood pressure – 110/70mmHg, respiratory rate – 34/min, SpO2 – 72% in room air; 98% with NIV. There were bilateral crepitations in all lung fields + no obvious abnormalities on CVS, CNS, and abdominal examination. POC ultrasound revealed multiple B-lines in all lung areas. Dilated IVC. The remaining cardiac, abdomen, and limb USGs were normal. ABG revealed Type 1 respiratory failure with elevated lactates. Bedside CXR and chest CT revealed diffuse bilateral lung infiltrates – not typical of pulmonary edema or pneumonia. Probable ARDS was mentioned. Blood samples had been sent for necessary investigations, including cultures and peripheral blood smear.

Management

Meanwhile, opinions were obtained from critical care consultants and pulmonologists regarding further management. Based on the clinical findings, it was decided to start the patient on broad-spectrum antibiotics (BSA), albumin transfusion, diuretics for the fluid overload status, and NIV for respiratory failure [all in suspicion of sepsis with MODS]. The patient was started on BSA before shifting to the ICU. Meanwhile, the blood reports arrived, suggestive of possible Myelodysplastic Syndrome (WBC – 95,000 cu.mm), Hb – 7g/dl. Peripheral Blood Smear report was Acute Myeloid Leukemia – possible M2 or M3.

The patient was immediately started on IV fluids, and oncology consultation was immediately obtained for chemotherapy initiation. Albumin and diuretics were withheld in suspicion of blast crisis and leukostasis / leukemic infiltration of the lungs. The patient was started on Cisplatin and other chemotherapeutic agents; bicarbonate infusion for urine alkalinization; allopurinol to treat hyperuricemia due to cytolysis; aggressive IV fluids for prevention of AKI due to chemotherapy and hyperuricemia [Tumour Lysis Syndrome]. Bone marrow biopsy was done during his hospital stay, which confirmed blast crisis AML-M3. His clinical condition improved considerably, and he was discharged from the hospital on Day 7.

Lessons Learnt

  1. Recognising leukostasis and hyperviscosity in the ED in an undiagnosed AML patient is extremely difficult. https://link.springer.com/chapter/10.1007/978-3-030-22445-5_3
  2. While considering different diagnoses based on clinical findings, always keep an open eye. Rare diseases present to the ED just like all others. https://www.medscape.com/viewarticle/860747_3
  3. Aggressive fluid management is needed in hyperviscosity syndrome. If we had started this patient on diuretics as planned, the blood would have become more viscous and lead to multisystem thrombosis. https://pubmed.ncbi.nlm.nih.gov/22915493/
  4. Increased metabolism in AML can present as pyrexia. With the other features of anemia, leucocytosis, petechiae, and anasarca, we are likely to diagnose this as sepsis. When in doubt, look through other causes of pyrexia (PUO). https://onlinelibrary.wiley.com/doi/full/10.1111/imj.13180
  5. Anasarca in leukemia does not warrant albumin transfusion as this may worsen fluid status. They may actually be in need of steroid therapy. https://www.hindawi.com/journals/crihem/2012/582950/
  6. Point of Care Lab testing is essential to reduce the number of diagnostic errors in the ED. https://acutecaretesting.org/en/articles/
Cite this article as: Gayatri Lekshmi Madhavan, India, "The Case of the Perplexing Crepitations," in International Emergency Medicine Education Project, June 14, 2021, https://iem-student.org/2021/06/14/the-case-of-the-perplexing-crepts/, date accessed: September 30, 2022

Recent Blog Posts By Gayatri L. Madhavan

From Missed Hemodialysis to Multiple Arrhythmias

From Missed Hemodialysis to Multiple Arrhythmias

Case Presentation

A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.

Vitals

HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)

ECG

ECG on presentation
Monomorphic ventricular tachycardia

He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.

In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.

ABG Findings

pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L

As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern. 

He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters. 

after hemodialysis

The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).

For the Inquisitive Minds

  1. The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
  2. His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
  3. Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
  4. Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
  5. What was the necessity for carrying out SLED for this patient?
  6. Why was this patient not immediately cardioverted in the ER?
  7. If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
  8. How differently would you have managed this patient?

Please give your answers and comments into "leave a reply" area below.

Cite this article as: Gayatri Lekshmi Madhavan, India, "From Missed Hemodialysis to Multiple Arrhythmias," in International Emergency Medicine Education Project, November 2, 2020, https://iem-student.org/2020/11/02/missed-hemodialysis/, date accessed: September 30, 2022