Background: Subarachnoid hemorrhage (SAH) is a neurological emergency associated with substantial morbidity and mortality. The present study was undertaken to evaluate the clinical presentation, radiological characteristics, and laboratory profile of patients with SAH admitted to a tertiary care centre in Central India. Method: This cross-sectional study included 100 patients aged ≥13 years with confirmed SAH. Demographic details, clinical presentation, laboratory parameters, radiological, treatment, complication, and outcome data were recorded. Associations were assessed using appropriate statistical tests, with ROC analysis and multivariable logistic regression used to evaluate predictors of mortality. Results: The largest age group was 41–50 years (23.0%), with 55.0% males and 58.0% rural residents. Thunderclap headache was the commonest symptom (60.0%), followed by neck rigidity (47.0%) and vomiting (45.0%). Hypertension was the commonest comorbidity (38.0%). Moderate GCS (9–12) was seen in 50.0%, while Hunt & Hess Grade IV (37.0%) and WFNS Grade IV (45.0%) predominated. Modified Fisher Grade 3 was most frequent (31.0%). Hyponatremia occurred in 19.0% and thrombocytopenia in 27.5%. On NCCT, basal cistern involvement was most common (74.0%); CT angiography identified aneurysms in 45.0%, predominantly involving the ACOM (60.0%). MRI showed SAH in 100.0% (22/22), while DSA detected aneurysms in 68.8% (11/16). Coiling was the commonest intervention (27.0%) and hydrocephalus was the most frequent complication (28.0%). Overall, 74.0% were discharged and 26.0% died. Modified Fisher grade was significantly associated with vasospasm (p=0.029), while GCS, WFNS grade, hypertension, diabetes, sodium status, and complications were significantly associated with outcome (p<0.05). The multivariable model showed good mortality discrimination (AUC=0.780), with GCS and WFNS grade as significant predictors. Conclusion: SAH showed considerable clinical and radiological heterogeneity with substantial in-hospital mortality. Early neurological severity assessment, identification of aneurysmal disease and complications, and prompt management of high-risk patients may improve outcomes.
Subarachnoid hemorrhage (SAH) is a life-threatening neurological emergency associated with high mortality and permanent disability.1 It is characterized by bleeding into the subarachnoid space between the arachnoid and pia mater.2 SAH may be traumatic, resulting from head injury, or spontaneous, most commonly caused by rupture of a cerebral aneurysm.3,4
SAH accounts for approximately 5% of all strokes worldwide and has a high case-fatality rate of 40–50%.5 Although age-standardized rates are declining globally, the absolute number of cases is increasing due to population growth and ageing.6 The incidence of aneurysmal SAH in India is generally lower than in Western countries and Japan, with considerable regional variation. Bhat et al. reported an SAH incidence of 13/100,000 persons/year in Kashmir7, while Indian studies have reported intracranial aneurysm prevalence ranging from 0.75–10.3%.8,9
However, SAH typically presents with a sudden “thunderclap” headache, often accompanied by vomiting, loss of consciousness, seizures, photophobia, and neck stiffness.10 Major complications include vasospasm, rebleeding, and raised intracranial pressure, contributing significantly to morbidity and mortality.11 Once a subarachnoid hemorrhage is suspected, a computed tomography of the head with the assistance of the Ottawa subarachnoid hemorrhage rule should be utilized as an initial diagnostic measure.12 If further investigation is needed, a CT angiography of the head or a lumbar puncture can be considered keeping risks and limitations in mind.13 Although several international studies have evaluated the clinical presentation, radiological findings, and laboratory profile of SAH, data from Central India remain limited. Therefore, present study was undertaken to evaluate the clinical presentation, radiological characteristics, and laboratory profile of patients with subarachnoid hemorrhage admitted to a tertiary care centre in Central India.
After obtaining Institutional Ethical Committee approval and written informed consent from guardians and/or patients, this hospital based, cross-sectional observational study was conducted in the Intensive Care Unit (ICU) and wards of the Medicine Department at a tertiary care center of central India during the time period of 1.5 years from November 2024 to May 2026. A total of 100 patients aged ≥13 years with SAH confirmed by clinical features and neuroimaging (CT/MRI/angiography) were included. Patients with incomplete records or those unwilling to participate were excluded.
Detailed demographic, clinical, comorbidities (e.g., hypertension, diabetes), lifestyle factors (e.g., smoking, alcohol use), and chief complaint (headache, vomiting, loss of consciousness, seizures, and focal neurological deficits), history of presenting illness, past medical history were recorded. Neurological severity was assessed using the Hunt and Hess Scale and Glasgow Coma Scale (GCS). Laboratory investigations included CBC, LFT, KFT, electrolytes, coagulation profile, blood sugar, HbA1c, lipid profile, blood culture, and HIV serology using standard automated laboratory methods. CSF analysis was performed when indicated. A Non-contrast CT scan (NCCT) was performed in all patients to confirm the diagnosis of SAH and identify the location of the hemorrhage and CT head angiography in most of the patients. MRI, and portable ultrasound digital subtraction angiography (DSA) performed where indicated. The Modified Fisher score and radiological findings were documented. ECG and 2D echocardiography were also assessed. Details of treatment, surgical intervention, complications such as vasospasm, rebleeding, and hydrocephalus, and in-hospital mortality were recorded.
Statistical Analysis
Data was entered in Microsoft Excel and analyzed using IBM SPSS Statistics version 20.0. Continuous variables were expressed as mean ± SD, while categorical variables were presented as frequencies and percentages. Normality was assessed using the Shapiro–Wilk test. Associations between categorical variables were assessed using the Chi-square test. A p-value <0.05 was considered statistically significant.
Among the 100 study participants, the largest proportion of cases belonged to the 41–50 years age group (23.0%), followed by 51–60 years (20.0%). Males constituted 55.0% of the participants, while females constituted 45.0%. Regarding residence, the majority of participants were from rural areas (58.0%), compared with 42.0% from urban areas. Regarding BMI, 60.0% were overweight (25–29.9 kg/m²), while 18.0% were obese (≥30 kg/m²), (Table 1).
Table 1: Socio-demographic characteristics of patients with SAH
| Characteristics | Frequency (n) | Percentage (%) | |
| Age Group (years) | ≤ 20 | 3 | 3.0 |
| 21–30 | 10 | 10.0 | |
| 31–40 | 15 | 15.0 | |
| 41–50 | 23 | 23.0 | |
| 51–60 | 20 | 20.0 | |
| 61–70 | 13 | 13.0 | |
| > 70 | 16 | 16.0 | |
| Gender | Male | 55 | 55.0 |
| Female | 45 | 45.0 | |
| Residence | Urban | 42 | 42.0 |
| Rural | 58 | 58.0 | |
| BMI (kg/m²) | 18.5–24.9 | 22 | 22.0 |
| 25–29.9 | 60 | 60.0 | |
| ≥ 30 | 18 | 18.0 | |
The most common presenting complaint was thunderclap headache (60%), followed by neck rigidity (47%), vomiting (45%), seizure (38%), loss of consciousness (35%), and focal neurological deficits (23%), (Figure 1).
Hypertension was the most prevalent comorbidity (38%), followed by diabetes mellitus (15%) and other conditions (13%) such as SLE, ADPKD, pulmonary tuberculosis, and chronic liver disease. Hyperlipidemia and prior stroke were less common (8% and 5%, respectively). Alcohol use was reported in 26% of participants and a history of medications (oral contraceptives, aspirin, streptokinase, and others) in 10%.
The neurological assessment showed that 50.0% of patients had moderate GCS scores. Hunt & Hess Grade IV (37.0%) and WFNS Grade IV (45.0%) were the most common grades. For the Modified Fisher scale, Grade 3 was the most frequent category (31.0%), followed by Grade 4 (25.0%), (Table 2).
Table 2: Neurological Assessment of Patients with SAH
| Neurological Assessment | Grade/Category | Frequency (n) | Percentage (%) |
| Glasgow Coma Scale (GCS) | Mild (13–15) | 33 | 33.0 |
| Moderate (9–12) | 50 | 50.0 | |
| Severe (3–8) | 17 | 17.0 | |
| Hunt & Hess Scale | Grade I | 06 | 6.0 |
| Grade II | 11 | 11.0 | |
| Grade III | 27 | 27.0 | |
| Grade IV | 37 | 37.0 | |
| Grade V | 19 | 19.0 | |
| WFNS Grade | Grade I | 12 | 12.0 |
| Grade II | 10 | 10.0 | |
| Grade III | 11 | 11.0 | |
| Grade IV | 45 | 45.0 | |
| Grade V | 22 | 22.0 | |
| Modified Fisher Grade | Grade 0 | 04 | 4.0 |
| Grade 1 | 16 | 16.0 | |
| Grade 2 | 24 | 24.0 | |
| Grade 3 | 31 | 31.0 | |
| Grade 4 | 25 | 25.0 |
Regarding vital parameters, most patients had a normal pulse rate (65.0%) and systolic blood pressure (70.0%). Tachycardia was present in 32.0% of patients, while 47.0% had a diastolic blood pressure >90 mmHg. Most patients were afebrile (79.0%), and 58.0% had a respiratory rate of 16–20 breaths/min.
The laboratory profile showed anemia in a substantial proportion of patients, particularly among females (82.22% had hemoglobin <12 g/dL). WBC counts were within the normal range in 68.0%, while thrombocytopenia was observed in 27.5%. Most patients had normal serum protein, bilirubin, liver enzymes, renal function, and electrolytes. Hyponatremia was present in 19.0% and hypokalemia in 27.0%. Coagulation parameters were largely within normal limits, although elevated PT, INR, and aPTT were observed in 22.5%, 12.5%, and 9.0% of patients, respectively, (Table 3).
Table 3: Laboratory Profile of Patients with SAH
| Parameters | Range | Frequency (n) | Percentage (%) |
| Hemoglobin – Males | ≤13 g/dL | 39 | 70.9 |
| 13–15 g/dL | 14 | 25.45 | |
| >16.5 g/dL | 02 | 3.63 | |
| Total | 55 | 100.0 | |
| Hemoglobin – Females | <12 g/dL | 37 | 82.22 |
| 12–15.5 g/dL | 07 | 15.55 | |
| >15.5 g/dL | 01 | 2.22 | |
| Total | 45 | 100.0 | |
| WBC Count | ≤4 × 10³/μL | 06 | 6.0 |
| 4–11 × 10³/μL | 68 | 68.0 | |
| >11 × 10³/μL | 26 | 26.0 | |
| Platelets | ≤150 × 10³/μL | 28 | 27.5 |
| 150–450 × 10³/μL | 72 | 72.5 | |
| >450 × 10³/μL | 00 | 0.0 | |
| Serum Protein | ≤6.0 g/dL | 25 | 25.0 |
| 6.0–8.3 g/dL | 73 | 72.5 | |
| >8.3 g/dL | 02 | 2.5 | |
| Bilirubin | ≤1.2 mg/dL | 88 | 87.5 |
| >1.2 mg/dL | 12 | 12.5 | |
| AST (SGOT) | ≤40 U/L | 72 | 72.0 |
| >40 U/L | 28 | 28.0 | |
| ALT (SGPT) | ≤40 U/L | 82 | 82.0 |
| >40 U/L | 18 | 18.0 | |
| ALP | ≤44 U/L | 10 | 10.0 |
| 44–147 U/L | 85 | 85.0 | |
| >147 U/L | 05 | 5.0 | |
| Urea | 15–40 (Normal) | 72 | 72.0 |
| >40 (Mild ↑) | 28 | 28.0 | |
| Creatinine | 0.6–1.2 (Normal) | 78 | 78.0 |
| >1.2 | 22 | 22.0 | |
| Sodium | < 135 (Hyponatremia) | 19 | 19.0 |
| 135–145 (Normal) | 77 | 77.0 | |
| > 145 (Hypernatremia) | 04 | 4.0 | |
| Potassium | < 3.5 (Hypokalemia) | 27 | 27.0 |
| 3.5–5.5 (Normal) | 65 | 65.0 | |
| > 5.5 (Hyperkalemia) | 08 | 8.0 | |
| PT (sec) | ≤11 sec | 33 | 32.5 |
| 11–13.5 sec | 45 | 45.0 | |
| >13.5 sec | 22 | 22.5 | |
| INR | ≤1.0 | 40 | 40.0 |
| 1.0–1.5 | 48 | 47.5 | |
| >1.5 | 12 | 12.5 | |
| aPTT (sec) | ≤35 sec | 91 | 91.0 |
| >35 sec | 09 | 9.0 |
ECG findings showed that 50.0% of patients had a normal ECG, while tachycardia (35.0%) was the most common abnormality. Bradycardia was observed in 10.0%, followed by LVH (18.0%), ST elevation (5.0%), LBBB (4.0%), and RVH (3.0%). RBBB was present in 2.0% of patients. On 2D echocardiography, 60.0% had normal findings, whereas concentric LVH and IHD were observed in 25.0% and 15.0% of patients, respectively.
Radiological evaluation showed that IPH (22.0%) and hydrocephalus (17.0%) were common NCCT findings, with the basal cisterns (74.0%) being the most frequently involved area. CT angiography identified aneurysms in 45.0% of patients, with ACOM being the commonest location (60.0%) and saccular morphology (70.0%) predominating. Among patients undergoing MRI (n=22), SAH was seen in all patients (100.0%), while acute infarction and hydrocephalus were observed in 50.0% and 54.5%, respectively. On DSA (n=16), aneurysm was the most common finding (68.8%), (Table 4).
Table 4: Radiological profile in patients with SAH
| Radiological Investigation | Finding/Category | Frequency (n) | Percentage (%) |
| NCCT Head Findings | Infarct | 08 | 8.0 |
| IPH (Intracerebral Hemorrhage) | 22 | 22.0 | |
| SAH + SDH | 12 | 12.0 | |
| Hydrocephalus | 17 | 17.0 | |
| IVH | 09 | 9.0 | |
| Area Involved on NCCT | Basal cisterns (around Circle of Willis) | 74 | 74.0 |
| Sylvian fissures | 56 | 56.0 | |
| Interhemispheric fissure | 47 | 47.0 | |
| Suprasellar cistern | 31 | 31.0 | |
| Ambient cisterns | 23 | 23.0 | |
| Cortical sulci (Convexity SAH) | 34 | 34.0 | |
| CT Head (A+V) | Aneurysm – No | 55 | 55.0 |
| Aneurysm – Yes | 45 | 45.0 | |
| Aneurysm Location | ACOM | 60 | 60.0 |
| PCOM | 10 | 10.0 | |
| MCA | 20 | 20.0 | |
| ACA | 10 | 10.0 | |
| Aneurysm Shape | Saccular | 70 | 70.0 |
| Others / Not specified | 30 | 30.0 | |
| Other CT Findings | SDH | 11 | 11.0 |
| IPH | 22 | 22.0 | |
| IVH | 09 | 18.0 | |
| Infarct | 08 | 8.0 | |
| Hydrocephalus | 28 | 28.0 | |
| Cerebral edema | 11 | 11.0 | |
| MRI Brain | Acute infarct | 11 | 50.0 |
| SAH | 22 | 100.0 | |
| Hydrocephalus | 12 | 54.5 | |
| DSA | Aneurysm | 11 | 68.8 |
| AVM (Arteriovenous Malformation) | 03 | 18.8 | |
| Normal study | 02 | 12.5 | |
| Total | 16 | 100.0 |
The most common surgical management was coiling (27.0%), followed by conservative management (23.0%) and neurosurgery (19.0%). Hydrocephalus (28.0%) was the most frequent complication. Aneurysm was the predominant etiology (48.0%). Among discharged patients (n=74), most had a good GCS of 14–15 (90.5%). Overall, 74.0% were discharged, while 26.0% died, (Table 5).
Table 5: Distribution of surgical management, complications, etiology, and outcomes
| Parameters | Category | Frequency (n) | Percentage (%) |
| Surgical Management | Conservative / No surgery | 23 | 23.0 |
| Neurosurgery | 19 | 19.0 | |
| Coiling | 27 | 27.0 | |
| Clipping | 16 | 16.0 | |
| Embolization | 15 | 15.0 | |
| Complications | Hydrocephalus | 28 | 28.0 |
| Vasospasm | 17 | 17.0 | |
| Rebleeding | 9 | 9.0 | |
| Hyponatremia | 14 | 14.0 | |
| Cardiac abnormalities | 11 | 11.0 | |
| None | 21 | 21.0 | |
| Etiology | Aneurysm | 48 | 48.0 |
| Intracranial hemorrhage | 18 | 18.0 | |
| CVST | 9 | 9.0 | |
| AVM / AV fistula | 5 | 5.0 | |
| Thrombocytopenia | 6 | 6.0 | |
| Coagulopathy | 5 | 5.0 | |
| Unknown | 9 | 9.0 | |
| GCS at Discharge | ≤8 (Severe) | 0 | 0.0 |
| 9–13 (Moderate) | 7 | 9.45 | |
| 14–15 (Mild/Good) | 67 | 90.5 | |
| Total | 74 | 100.0 | |
| Outcome | Discharged | 74 | 74.0 |
| Death | 26 | 26.0 |
GCS categories were not significantly associated with gender (p=0.97) or age group (p=0.999). However, a statistically significant association was observed between Hunt & Hess grade and GCS category (p=0.017), with higher Hunt & Hess grades showing a greater proportion of moderate-to-severe GCS scores, (Table 6).
Table 6: Association of gender, age group, and Hunt & Hess grade with GCS categories
| Parameters | Mild | Moderate | Severe | P value | |
| Gender | Male (55%) | 18 | 28 | 9 | 0.97 |
| Female (45%) | 15 | 22 | 8 | ||
| Age Group (years) | ≤20 | 01 | 01 | 01 | 0.999 |
| 21–30 | 03 | 05 | 02 | ||
| 31–40 | 05 | 07 | 03 | ||
| 41–50 | 08 | 11 | 04 | ||
| 51–60 | 07 | 10 | 03 | ||
| 61–70 | 04 | 07 | 02 | ||
| >70 | 05 | 09 | 02 | ||
| Hunt & Hess Grade | Grade I | 05 | 01 | 00 | 0.017 |
| Grade II | 09 | 02 | 00 | ||
| Grade III | 04 | 15 | 00 | ||
| Grade IV | 10 | 15 | 02 | ||
| Grade V | 05 | 17 | 15 | ||
The prevalence of vasospasm increased with higher Modified Fisher grades: 0/4 (0.0%) in Grade 0, 1/16 (6.3%) in Grade 1, 3/24 (12.5%) in Grade 2, 6/31 (19.4%) in Grade 3, and 7/25 (28.0%) in Grade 4. Overall, vasospasm was present in 17/100 (17.0%) patients and absent in 83/100 (83.0%). The association was statistically significant (χ² = 10.8, df = 4, p = 0.029).
The analysis showed that clinical complications, admission GCS, WFNS grade, hypertension, diabetes mellitus, and sodium status were significantly associated with patient outcomes (p<0.05). Mortality was higher among patients with hydrocephalus, moderate-to-severe GCS scores, and higher WFNS grades, particularly Grade V. Hypertension (p=0.015), diabetes mellitus (p=0.043), and sodium status (p=0.043) were also significantly associated with mortality, (Table 7).
Table 7: Association of clinical and laboratory parameters with patient outcome
| Parameters | Discharged (n=74) | Death (n=26) | P value | |
| Complications | Hydrocephalus | 17 | 11 | 0.002 |
| Vasospasm | 11 | 06 | ||
| Rebleeding | 4 | 05 | ||
| Hyponatremia | 13 | 01 | ||
| Cardiac abnormalities | 08 | 03 | ||
| No complications | 21 | 00 | ||
| GCS Category | Mild (13–15) | 33 | 00 | <0.001 |
| Moderate (9–12) | 32 | 18 | ||
| Severe (3–8) | 09 | 08 | ||
| WFNS Grade | Grade I | 12 | 00 | <0.001 |
| Grade II | 10 | 00 | ||
| Grade III | 10 | 01 | ||
| Grade IV | 34 | 11 | ||
| Grade V | 08 | 14 | ||
| Hypertension | Present | 30 | 08 | 0.015 |
| Absent | 44 | 18 | ||
| Diabetes Mellitus | Present | 08 | 07 | 0.043 |
| Absent | 66 | 19 | ||
| Sodium Status | Hyponatremia (<135 mEq/L) | 10 | 09 | 0.043 |
| Normal (135–145 mEq/L) | 61 | 16 | ||
| Hypernatremia (>145 mEq/L) | 03 | 01 | ||
Involvement of the suprasellar cistern (χ²=6.65, p=0.010) and ambient cisterns (χ²=7.57, p=0.006) was significantly associated with outcome, whereas basal cistern, sylvian fissure, interhemispheric fissure, and cortical sulci involvement showed no significant association.
ROC analysis showed that the multivariable model had the highest predictive performance for in-hospital mortality (AUC = 0.780). Among individual parameters, admission GCS showed the best discrimination, followed by WFNS grade, while Modified Fisher grade, serum sodium, and age demonstrated limited predictive ability, (Table 8 & figure 2).
Table 8: ROC curve analysis of clinical parameters for predicting mortality
| Parameters | AUC | Optimal Cut-off | Sensitivity (%) | Specificity (%) |
| Admission GCS Score | 0.708* | ≤12 (clinical cut-off recommended) | — | — |
| WFNS Grade | 0.620 | ≥5 | 37.0 | 83.6 |
| Modified Fisher Grade | 0.506 | ≥3 | 59.3 | 45.2 |
| Serum Sodium (mEq/L) | 0.584 | ≤128 | 100.0 | 15.1 |
| Age (years) | 0.442 | ≥71 | 25.9 | 86.3 |
| Multivariable Prediction Model | 0.780 | — | — | — |
A multivariable logistic regression model including age, admission GCS, WFNS grade, Modified Fisher grade, hypertension, diabetes mellitus, and serum sodium showed good predictive performance for in-hospital mortality, with an AUC of 0.780, indicating acceptable discriminative ability, (Table 9).
Table 9: Multivariate logistic regression analysis for predictors of in-hospital mortality among patients with SAH
| Variable | OR | CI Lower | CI Upper | p-value |
| Age | 0.978779 | 0.950479 | 1.007923 | 0.151914 |
| GCS | 1.374864 | 1.113013 | 1.698320 | 0.003145 |
| WFNS Grade | 1.625168 | 1.047174 | 2.522187 | 0.030348 |
| Modified Fisher Grade | 0.914124 | 0.584381 | 1.429928 | 0.694072 |
| Comorbidities-1: Hypertension | 1.688464 | 0.609773 | 4.675363 | 0.313440 |
| Comorbidities-2: Diabetes Mellitus | 0.305968 | 0.056083 | 1.669232 | 0.171287 |
| Sodium | 1.053305 | 0.962733 | 1.152399 | 0.257607 |
In the present study, 72% of patients were aged >40 years, with the highest proportion in the 41–50-year group (23%), comparable to Sadasivam et al.14 A slight male predominance (55%) was observed. The rural predominance (58%) may reflect differences in healthcare access, referral patterns, and risk-factor exposure. Overweight (60%) and obesity (18%) indicated a substantial cardiometabolic risk burden, similar to Ritter et al.15 Thunderclap headache (60%) was the commonest symptom, followed by neck rigidity, vomiting, seizures, loss of consciousness, and focal deficits, consistent with Sadasivam et al14 and Sweeney et al.16 [43]. Hypertension (38%) and diabetes (15%) were the leading comorbidities. Tachycardia, elevated blood pressure, and fever were also commonly observed. Alcohol use observed in 26% and medication history in 10%. These findings in agreement with Ewbank et al study.17
The 50% of cases had moderate GCS (9–12) and 17% had severe impairment, this differs from studies by Mistry et al18 and Al-Mistarehi et al19, where most patients presented with GCS 15 or mild neurological impairment. Similarly, 83% had Hunt and Hess Grades III–V, with Grade IV being most common (37%), while 67% had WFNS Grades IV–V. This greater proportion of poor-grade SAH was also reported in previous studies.14,18,19 Regarding radiological severity, 80% had Modified Fisher Grades 2–4, indicating a substantial subarachnoid blood burden. This finding is comparable to observations by Komiyama et al20 and Zhao et al.21
The present study showed a high prevalence of anemia, affecting 70.9% of males and 82.2% of females, indicating substantial hematological stress in patients with SAH. Most patients had preserved liver and renal function, with normal serum protein and bilirubin levels. Hyponatremia (19%) and hypokalemia (27%) were common electrolyte abnormalities and were comparable to findings reported by Zhao et al21. Abnormal coagulation parameters, including prolonged PT and elevated INR, were observed in a minority of patients.
50% of cases showing abnormal ECG findings, predominantly tachycardia (35%) and ST-segment elevation (5%), consistent with the cardio-neurological changes reported by Subah et al.22 On NCCT, blood was most commonly distributed in the basal cisterns (74%), followed by the Sylvian (56%) and interhemispheric fissures (47%), in agreement with patterns described by Komiyama et al.20 IVH was observed in 9%, while IPH (22%) and SDH (12%) indicated substantial associated intracranial bleeding. Hydrocephalus occurred in 17% of cases. MRI demonstrated SAH in all 22 patients, with acute infarction and hydrocephalus in 50% and 54.5%, respectively. DSA identified aneurysms in 68.8%, supporting its role as the definitive vascular imaging modality and consistent with findings reported by Gusdon et al.23
The definitive aneurysm treatment included coiling (27%), clipping (16%), and embolization (15%), reflecting the increasing preference for endovascular approaches in SAH management, consistent with findings reported by Rossi et al.24 Hydrocephalus (28%) and vasospasm (17%) were the most frequent complications, and aneurysm was the leading etiology (48%). Overall, 74% of patients were discharged, and among survivors, 90.5% had a good/mild GCS (14–15) at discharge, indicating favorable neurological recovery among those who survived the acute phase.
There was no significant association between gender and admission GCS (p=0.97) or between age group and GCS category (p=0.999). A significant association was observed between Hunt & Hess grade and admission GCS (p=0.017), with higher Hunt & Hess grades showing a greater proportion of moderate-to-severe GCS scores. These finding are consistent with which is consistent with the findings of Mistry et al18.
Clinical complications, particularly rebleeding and hydrocephalus, were associated with higher mortality, whereas patients without complications had favorable outcomes. Admission neurological severity was strongly associated with mortality, with all patients having mild GCS surviving, while mortality increased with worsening GCS and WFNS grades, supporting the prognostic value of these scales reported by Mistry et al.18 A significant association was observed between Modified Fisher grade and vasospasm (p=0.029), with vasospasm increasing from 0% in Grade 0 to 28% in Grade 4. This dose-dependent relationship between subarachnoid blood burden and vasospasm is consistent with Komiyama et al20. Hypertension was not significantly associated with mortality, in contrast, diabetes mellitus was significantly associated with higher mortality (p=0.043), consistent with findings reported by Lampmann et al.25 Hyponatremia was also associated with poorer outcome, supporting the recognized prognostic importance of electrolyte disturbances in SAH.
The involvement of the suprasellar cistern (p=0.010) and ambient cisterns (p=0.006) was significantly associated with patient outcome, whereas involvement of the basal cisterns, Sylvian fissures, interhemispheric fissure, and cortical sulci was not statistically significant. These findings suggest that the anatomical distribution and extent of subarachnoid blood may influence prognosis, consistent with observations reported by Zhao et al21.
The present study was limited by its cross-sectional design, convenient sampling, single-center setting, and relatively small sample size, which may limit generalizability. The absence of long-term follow-up and longitudinal data restricted assessment of functional recovery and late complications. In addition, transcranial Doppler (TCD) was unavailable, potentially resulting in under-detection of vasospasm. Future studies should therefore use larger, multicenter prospective cohorts with standardized sampling, serial assessments, TCD monitoring, and long-term follow-up to better evaluate complications, functional outcomes, and quality of life in patients with SAH.
Subarachnoid hemorrhage remains a devastating neurological emergency associated with high mortality and morbidity. The present study provides the first comprehensive profile of SAH in Central India, offering actionable insights for clinicians and policymakers. Most patients presented with moderate-to-severe neurological impairment, and higher admission GCS, WFNS, and Modified Fisher grades were associated with poorer outcomes and increased complications. Hydrocephalus and vasospasm were the commonest complications, while aneurysm was the leading etiology. By recognizing high-risk features (age >40, hypertension, diabetes, severe admission scores), improving early diagnosis, and optimizing complication management, we can improve outcomes for SAH patients in this region and beyond.
1. D'Souza S. Aneurysmal Subarachnoid Hemorrhage. J Neurosurg Anesthesiol. 2015 Jul;27(3):222-40.
2. Ziu E, Khan Suheb MZ, Mesfin FB. Subarachnoid Hemorrhage. [Updated 2023 Jun 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK441958/
3. Griswold D.P., Fernandez L., Rubiano A.M. Diagnosis and Management of Traumatic Subarachnoid Hemorrhage: Protocol for a Scoping Review. JMIR Res. Protoc. 2021;10:e26709.
4. Sanicola HW, Stewart CE, Luther P, Yabut K, Guthikonda B, Jordan JD, Alexander JS. Pathophysiology, Management, and Therapeutics in Subarachnoid Hemorrhage and Delayed Cerebral Ischemia: An Overview. Pathophysiology. 2023 Sep 14;30(3):420-442.
5. Li W, Yang H, Rui F, Ruan X, Xiong J, Chen L. Systematic analysis of the global, regional, and national burden of subarachnoid hemorrhage from 1990 to 2021. PLoS One. 2025 May 29;20(5):e0323453.
6. Chalouhi N, Hoh BL, Hasan D. Review of cerebral aneurysm formation, growth, and rupture. Stroke. 2013;44(12):3613-3622.
7. Bhat AR, AfzalWani M, Kirmani AR. Subarachnoid hemorrhage in Kashmir: Causes, risk factors, and outcome. Asian J Neurosurg 2011;6:57‐71.
8. Koshy L, Easwer HV, Premkumar S, Alapatt JP, Pillai AM, Nair S, Bhattacharya RN, Banerjee M. Risk factors for aneurysmal subarachnoid hemorrhage in an Indian population. Cerebrovascular Diseases. 2010 Feb 1;29(3):268-74.
9. Etminan N, Chang HS, Hackenberg K, De Rooij NK, Vergouwen MD, Rinkel GJ, Algra A. Worldwide incidence of aneurysmal subarachnoid hemorrhage according to region, time period, blood pressure, and smoking prevalence in the population: a systematic review and metaanalysis. JAMA neurology. 2019 May;76(5):588-97.
10. Bracard S, Schmitt E. Vasospasm and delayed consequences. IntervNeuroradiol. 2008 Sep 1;14 Suppl 1(Suppl 1):17-22.
11. Perry JJ, Stiell IG, Sivilotti ML, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248–55.
12. Guideline NG228 NI. Subarachnoid haemorrhage caused by a ruptured aneurysm: diagnosis and management. Methods. 2022 Nov.
13. Marcolini E, Hine J. Approach to the Diagnosis and Management of Subarachnoid Hemorrhage. West J Emerg Med. 2019 Mar;20(2):203-211.
14. Sadasivam AS, Nathan B, Anbazhagan SP. Clinical Profile and Outcome in Patients with Spontaneous Subarachnoid Hemorrhage from a South Indian Tertiary Centre: A Prospective Observational Study. Asian J Neurosurg. 2023 Mar 27;18(1):80-87.
15. Ritter H, Halama D, Arlt F, Stockert A, Werdehausen R, Hoffmann KT, Richter C. Aneurysmal subarachnoid hemorrhage-risk score—impact of pre-existing cardiovascular risk factors on functional patient outcomes. Frontiers in Neurology. 2026 Mar 11;17:1781480.
16. Sweeney K, Silver N, Javadpour M. Subarachnoid haemorrhage (spontaneous aneurysmal). BMJ ClinEvid. 2016 Mar 17;2016:1213.
17. Ewbank F, Gaastra B, Hall S, Galea I, Bulters D. Risk of subarachnoid haemorrhage reduces with blood pressure values below hypertensive thresholds. Eur J Neurol. 2024 Jan;31(1):e16105.
18. Mistry AM, Saver J, Mack W, Kamel H, Elm J, Beall J. Subarachnoid Hemorrhage Trials: Cutting, Sliding, or Keeping mRS Scores and WFNS Grades. Stroke. 2024 Mar;55(3):779-784.
19. Al-Mistarehi AH, Elsayed MA, Ibrahim RM, Elzubair TH, Badi S, Ahmed MH. Clinical Outcomes of Primary Subarachnoid Hemorrhage: An Exploratory Cohort Study from Sudan. Neurohospitalist.0 2022 Apr;12(2):249-263.
20. Komiyama M. Misunderstanding of Fisher's grouping system for computed tomography evaluation of aneurysmal subarachnoid haemorrhage. IntervNeuroradiol. 2019 Dec;25(6):653-654.
21. Zhao D, Li Y, Cui J. The factors associated with the modified Fisher grade in patients with aneurysmal subarachnoid hemorrhage. Front Physiol. 2024 Jul 17;15:1373925.
22. Subah G, Patel R, Nolan B, Fortunato M, Lui A, Uddin A et al. Acute kidney injury in subarachnoid hemorrhage: Exploring its clinical significance and prognostic implications. J Stroke Cerebrovasc Dis. 2024 Sep;33(9):107843.
23. Gusdon AM, Savarraj JPJ, Shihabeddin E, Paz A, Assing A, Ko SB, McCullough LD, Choi HA. Time Course of Peripheral Leukocytosis and Clinical Outcomes After Aneurysmal Subarachnoid Hemorrhage. Front Neurol. 2021 Jul 26; 12:694996.
24. Rossi YI, Bolner G, Dall'Acqua JC, de Oliveira FD, Zacaria LV, Denicol TL et al. Comparative outcomes of coil embolization and surgical clipping in elderly patients with subarachnoid hemorrhage: a systematic review and meta-analysis. Neurosurg Rev. 2025 Aug 4;48(1):587.
25. Lampmann T, Hadjiathanasiou A, Asoglu H, Wach J, Kern T, Vatter H, Güresir E. Early Serum Creatinine Levels after Aneurysmal Subarachnoid Hemorrhage Predict Functional Neurological Outcome after 6 Months. J Clin Med. 2022 Aug 15;11(16):4753.