European Journal of Cardiovascular Medicine

Sepsis is a complex, life threatening clinical syndrome characterized by organ dysfunction caused by a dysregulated host response to the infection. It is one of the most difficult conditions to treat in modern intensive care medicine and is still one of the main causes of death and illness around the world. The Third International Consensus Definitions for Sepsis and Septic Shock said that sepsis is organ dysfunction that threatens life because the host's response to infection is out of control. This shows how important the interaction between the host and the pathogen and the systemic inflammatory response are in the progression of the disease.1

Septic shock is considered the most severe subset of sepsis and is clinically identified by persistent hypotension requiring vasopressor therapy and elevated serum lactate levels despite adequate fluid resuscitation. This stage reflects profound circulatory, cellular, and metabolic abnormalities that substantially increase mortality risk. Epidemiological studies from developed countries estimate the incidence of septic shock to be approximately 8.2 per 100 intensive care admissions, with reported mortality rates ranging between 30% and 60% depending on severity, comorbid conditions, and availability of early goal‑directed therapy.2,3 Despite advances in antimicrobial therapy, organ support techniques, and critical care monitoring, septic shock continues to account for a major proportion of deaths in intensive care units worldwide.

The pathophysiology of sepsis entails a highly intricate interplay among inflammatory, immunologic, endocrine, and metabolic pathways4. When an infection happens, the immune system of the host works to get rid of the pathogens. In sepsis, this response becomes unregulated, which causes too many pro-inflammatory mediators to be released, damage to the endothelium, problems with the microvasculature, and problems with the body's ability to use oxygen. This cascade ultimately results in the cellular injury, organ dysfunction, and the hemodynamic instability5-6.

AIMS AND OBJECTIVES OF THE STUDY

AIM: To determine the incidence of adrenal insufficiency in ICU admitted patients with septic shock

OBJECTIVES

• To evaluate the incidence of adrenal insufficiency in ICU admitted patients with septic shock.
• To identify the correlation between serum cortisol levels and mortality in patients with septic shock.

MATERIALS AND METHODS The data was collected from the patients who are admitted with septic shock in Medical Intensive Care Unit in department of General Medicine at HIMS, Hassan and Department of Anaesthesiology SBMPMC( BLDE University) Vijayapura, who met inclusion and exclusion criteria. After getting institutional ethical clearance.Sample Size: 70 patients. Patients who are admitted with septic shock in Medical Intensive Care Unit in department of General Medicine at HIMS, Hassan and Department of Anaesthesiology SBMPMC ( BLDE University) Vijayapura were selected according to the inclusion and exclusion criteria mentioned below Inclusion Criteria • Patients who are more than 18 years of age and less than 65 years of age. • Meeting the criteria for sepsis by the Sepsis Guidelines 2021. • With systolic BP <90 mmHg despite fluid therapy and more than one hour of vasopressor requirement • Within 48 hours of hospital admission Exclusion Criteria • Patients are less than 18 years of age and more than 65 years. • Pregnant women/ lactating women. • Patients with renal failure • Patients with cardiac disease • Patients with hepatic failure • Patients with disseminated tuberculosis • Patients who are already on steroid therapy SAMPLE SIZE ESTIMATION The data will be collected from people who are admitted with septic shock in Medical Intensive Care Unit in department of General Medicine at HIMS, Hassan. In the Annane et al.,13 study, there is an incidence of 76.3% of relative adrenal insufficiency in Septic Shock. • Sample size (n) = Z2 x p x q • δ2 • where Z= 1.96. • p= 76.3%=76.3/100=0.763. • q=(1-p) =0.237. • δ=allowable error=10%=0.1 • n = (1.96)2 x 0.763 x 0.237 n = 69 • (0.1)2 • Estimated sample size = 70 METHODOLOGY AND FOLLOW-UP After getting approval from Institutional ethics committee, written informed consent was taken. Patients who are admitted with septic shock in Medical Intensive Care Unit in department of General Medicine were selected according to inclusion and exclusion criteria. The aims and objectives of the intended study was properly explained to the subject. Data was be collected as per the proforma sheet. A detailed history and complete general examination, regional examination, systemic examination and radiologic examination was performed on every subject participating in the study as per predesigned proforma. Required information and test results to assess the SOFA score was obtained for all these patients. To estimate serum cortisol levels, blood sample for serum cortisol was taken for all these patients under study within 48 hours of hospital admission. Serum cortisol was tested in biochemistry lab using ‘ARCHITECT’(registered) equipment, ARCHITECT cortisol is a chemiluminescent microparticle immunoassay (CMIA) with ARCHITECT cortisol 8D15 kit contents. STATISTICAL METHODS Data was entered on Microsoft Excel (Windows 10; Version 2025) and analyses was done using the Statistical Package for Social Sciences (SPSS) for Windows software (version 29.0; SPSS Inc, Chicago). Descriptive analysis and inferential analysis are done. Categorical variables (sex, comorbidities, habits, SOFA categories and urine findings) were summarised as frequency and percentage. Continuous variables (age, anthropometry, vitals and laboratory parameters) were expressed as mean ± standard deviation with minimum–maximum values. The association between SOFA score and biochemical parameters was assessed using Spearman’s rank correlation (rho). Correlation coefficients were interpreted as strong, moderate or weak. The results were presented in the tables and figures graphically, including the scatter plots for the key correlations such as the HbA1c, glucose and cortisol versus SOFA. p-value of less than 0.05 was considered statistically significant.

A total of 560 patient data

Table 1: Hormonal and Organ Dysfunction Scores

Serum cortisol levels among the participants ranged from 0.33 to 19.93 µg/dL, with a mean value of 10.13 ± 4.79 µg/dL. The wide variation in cortisol levels reflects differing stress responses among the study participants. The Sequential Organ Failure Assessment (SOFA) score ranged from 0 to 4, with a mean score of 2.31 ± 1.45. This indicates mild to moderate organ dysfunction in a subset of cases. Collectively, these parameters provide insight into the hormonal response and overall organ involvement in the study population.

Table 2: Distribution of SOFA Scores among Study Participants

The distribution of Sequential Organ Failure Assessment (SOFA) scores among the study participants showed varying degrees of organ dysfunction. A SOFA score of 0 was observed in 12 participants (17.1%), indicating no organ dysfunction. Scores of 1 and 2 were noted in 10 (14.3%) and 11 participants (15.7%), respectively, reflecting mild organ involvement. Moderate organ dysfunction was more common, with 18 participants (25.7%) having a SOFA score of 3. The highest proportion of participants, 19 (27.1%), had a SOFA score of 4, indicating more severe organ dysfunction. Overall, a substantial proportion of the study population exhibited moderate to severe organ dysfunction.

Table 3: Spearman’s correlation between SOFA score serum parameters

HbA1c

HbA1c showed a strong positive correlation with SOFA score (r = 0.692, p < 0.001). This indicates that higher HbA1c levels were associated with higher SOFA scores, reflecting greater organ dysfunction. The association was statistically highly significant, suggesting a meaningful relationship between long-term glycaemic control and disease severity.

Fasting Blood Sugar (FBS)

FBS demonstrated a moderate positive correlation with SOFA score (r = 0.400, p = 0.001). Elevated fasting glucose levels were associated with increasing SOFA scores. This significant correlation suggests that poor fasting glycaemic control may contribute to worsening organ dysfunction.

Post-Prandial Blood Sugar (PPBS)

PPBS showed a moderate positive correlation with SOFA score (r = 0.382, p = 0.001). Higher post-prandial glucose values were linked with higher SOFA scores. The statistically significant association highlights the impact of post-meal hyperglycaemia on disease severity

The mean age of the participants was 42.63 ± 13.07 years, which is younger than the average age of people with septic shock in the West, where the average age is usually over 60 years (2,3). Martin et al. showed that both the number of cases and the number of deaths rise sharply after age 65.7 The younger mean age in the present study may reflect the regional demographics and the study’s exclusion criteria.8

The study population comprised 52.9% males and 47.1% females. This distribution is similar to what Angus et al. found in their study of severe sepsis cohorts, where males made up 52–55% of the participants. Studies of the incidence of diseases around the world also show a similar pattern of slightly more men than women.9

The Renal dysfunction was indicated by the mean serum creatinine level of 4.19 ± 1.51 mg/dL, implying the substantial renal involvement. Schrier and Wang documented the acute renal failure in as many as 51% of the septic shock patients, which corresponds with the renal impairment noted in this cohort10.

The Metabolic acidosis was suggested by the reduced bicarbonate levels of (15.35 ± 3.12 mEq/L). Annane et al. emphasized that the lactic acidosis and the cellular metabolic failure are key components of the septic shock physiology11. These metabolic changes may further influence cortisol metabolism and adrenal responsiveness.

Trials of steroid therapy have yielded inconclusive outcomes. Minneci et al. found that corticosteroids helped shock reversal but not always survival. Lefering and Neugebauer talked about the risks that come with high-dose steroid therapy that depend on the dose. The cortisol profile in this study endorses selective and evidence-based steroid utilization over empirical administration12.

Indian literature is still not very broad. Chacko et al. showed that septic ICU patients had subclinical hypocortisolemia, and Visvanathan et al. showed that low-dose corticosteroids had good effects on blood flow in burn sepsis. This study contributes significant regional evidence concerning adrenal insufficiency in adult septic shock13.

Overall, the current findings validate that adrenal dysfunction is prevalent in septic shock and is associated with parameters of organ dysfunction. These results are in line with what has been found in other international and Indian studies. They also show how important it is to check the endocrine system in critically ill septic patients14.

The findings of this study demonstrate that a considerable proportion of patients with septic shock exhibit suboptimal cortisol response during critical illness. The mean serum cortisol level observed was lower than expected for severe physiological stress, suggesting the presence of relative adrenal insufficiency or critical illness‑related corticosteroid insufficiency in a subset of patients. This endocrine dysfunction appears to coexist with organ impairment and hemodynamic instability.

In the present study, the incidence of the adrenal insufficiency among the ICU-admitted patients with septic shock was approximately 84% (about 59 out of 70 patients) based on a serum cortisol cut-off value of <15 µg/dL. This finding indicates that a substantial proportion of critically ill septic shock patients exhibited inadequate adrenal stress response during the early phase of illness

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