Case 1.1
Monica Fawzy in Plastic Surgery Vivas for the FRCS(Plast), 2023
You’ve mentioned SIRS, ARDS, and DIC. What is the pathophysiology of these?Systemic inflammatory response syndrome is the clinical manifestation of dysregulated immune responses to infectious and non-infectious stimuli. It involves activation of the inflammatory cascade – with its humoral and cellular responses and complement and cytokine cascades. This may culminate in multi-organ failure, if left untreated.Acute respiratory distress syndrome is a non-cardiogenic pulmonary oedema where an inflammatory or mechanical insult causes endothelial cell dysfunction with leakage of cells and inflammatory exudate into the alveoli. This affects lung function with consequent hypoxia, increased work of breathing, atelectasis, and lung fibrosis.Disseminated intravascular coagulation is a disorder characterized by generalized widespread activation of coagulation, with thrombotic complications and diffuse haemorrhage due to consumption of platelets and coagulation factors.
Emergency Surgery
Tjun Tang, Elizabeth O'Riordan, Stewart Walsh in Cracking the Intercollegiate General Surgery FRCS Viva, 2020
What is SIRS?Systemic inflammatory response syndromeAny two of: Heart rate > 90 beats per minuteTemperature < 36°C or > 38°CWhite cell count <4 × 109/L or > 10 × 109/LRespiratory rate > 20 breaths per minute or PaCO2 <32 mmHgThis is caused by cytokine release in response to trauma, inflammation or infection.The SIRS criteria are non-specific and must be interpreted within the clinical context.
Transfusion in Trauma
Kenneth D Boffard in Manual of Definitive Surgical Trauma Care: Incorporating Definitive Anaesthetic Trauma Care, 2019
Despite the extensive list quoted above, there is limited evidence regarding the risks of pRBC transfusion, although pRBC transfusion is an independent risk factor for: Increased nosocomial infections (wound infection, pneumonia, sepsis).Multiple organ failure and systemic inflammatory response syndrome.Longer ICU and hospital length of stay, increased complications, and increased mortality.Pre-storage leukocyte depletion of RBC transfusion reduces complication rates, some studies showing a reduction in infectious complications.There is a relationship between transfusion and TRALI and ARDS.Transfusion and pRBC and FFP increase the risk for DVT in trauma patients.
Assessment of COVID-19 deaths from cardiological perspective
Published in Acta Cardiologica, 2022
Timor Omar, Muammer Karakayalı, Gökhan Perincek
As the exact mechanism has remained dusty, it is estimated that cardiological involvement and elevation of troponin in patients with COVID-19 come of various pathogenesis rather than typical large coronary artery occlusion [10,11]. Possible mechanisms are hypothesised as follows: 1) direct damage of cardiomyocytes from SARS-CoV-2; 2) hypoxia-induced myocardial injury. Similarly, in our study, lower oxygen saturation levels were noted in the non-survivor and cardiac injury groups; 3) the cardiac microvascular damage caused by vessel hyperpermeability and angio-spasm under the condition of inflammation and 4) the systemic inflammatory response syndrome, such as the cytokine storm in critically ill patients [12,13]. In any case, ECG abnormalities, elevated hs-TnT and ProBNP values are a manifestation of cardiac involvement [10, 14], and when considered together with clinical and laboratory findings, provides significant prognostic data.
A bite difficult to heal: Pasteurella multocida induced decompensated hepatic cirrhosis
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Hiren Patel, Nirali Patel, Harsh Patel, Robert Dobbin Chow
Initial laboratory tests were done in the emergency department (see Table 1). Laboratory work revealed an increase in creatinine to 1.5 mg/dL from baseline of 0.8 mg/dL and a drop in hemoglobin to 6.7 g/dL from baseline of 11 g/dL. Abdominal CT scan with intravenous (IV) contrast was consistent with hepatic cirrhosis along with a heterogeneous and nodular liver, portal hypertension with an enlarged portal vein, and gastric varices (see Figure 2). A CT scan of the right lower extremity was also performed, which showed cellulitis without abscess or gas formation. The patient received IV infusion of octreotide, packed red blood cells and platelets, and broad-spectrum antibiotics. Given the patient’s tachycardia and leukocytosis, he met two of four criteria for the systemic inflammatory response syndrome (SIRS). In addition to SIRS, given elevated lactate, hepatic encephalopathy, respiratory failure and concern for bleeding varices in setting of decompensated cirrhosis, patient was admitted to the intensive care unit (ICU).
An integrative understanding of the large metabolic shifts induced by antibiotics in critical illness
Published in Gut Microbes, 2021
Andrea Marfil-Sánchez, Lu Zhang, Pol Alonso-Pernas, Mohammad Mirhakkak, Melinda Mueller, Bastian Seelbinder, Yueqiong Ni, Rakesh Santhanam, Anne Busch, Christine Beemelmanns, Maria Ermolaeva, Michael Bauer, Gianni Panagiotou
Critical illness leads to the admission of more than 5 million patients per year to intensive care units (ICUs) in the United States alone. Intensive or invasive monitoring of ICU patients accounts for approximately 20% of the total US hospital cost, while the worldwide death rates for critically ill patients are increasing at a higher rate than any other common cause of death 1. Almost half of ICU patients show symptoms related to an initial systemic inflammatory response syndrome (SIRS).2 However, besides inflammation, signs of immune exhaustion or ‘paralysis’ might occur simultaneously.3 A disbalance of pro- and anti-inflammatory responses can lead to an increased risk of infection 4 and related sepsis, which are responsible for nearly 60% of deaths in ICUs and account for approximately 40% of ICU costs.5
Related Knowledge Centers
- Acute Kidney Injury
- Immunology
- Inflammation
- Infection
- Multiple Organ Dysfunction Syndrome
- Immune Response
- Insult
- Anti-Inflammatory
- Shock
- Pathogenic Bacteria