Tetanus with autonomic dysfunction in an elderly diabetic patient with restrictive cardiomyopathy and implanted pacemaker: A fatal outcome

Samyuktha D V1*, Aarthi2

1Group Clinical Pharmacist, Kauvery Hospital, Trichy, Tamil Nadu

2Clinical Pharmacist, Kauvery Hospital, Cantonment, Trichy, Tamil Nadu

*Correspondence

Abstract

Tetanus remains a life-threatening, vaccine-preventable disease, particularly dangerous in elderly individuals with significant comorbidities. We report a 70-year-old female with diabetes mellitus (DM), restrictive cardiomyopathy, sinus node dysfunction, and a previously implanted VVIR MRI-compatible pacemaker, who presented with acute-onset trismus and dysphagia following a thorn prick injury. Despite prompt diagnosis and aggressive multi-disciplinary management including tetanus immunoglobulin, metronidazole, tracheostomy, mechanical ventilation, muscle relaxants, and vasopressors for autonomic dysfunction, the patient succumbed on hospital day eleven due to cardiogenic shock, multiorgan dysfunction, and uncontrolled autonomic instability. This case highlights the catastrophic consequences of delayed wound management, the challenges of managing severe tetanus in high-risk patients, and the importance of universal tetanus immunization.

Keywords: Tetanus; Autonomic dysfunction; Restrictive cardiomyopathy; Pacemaker; Trismus; Mechanical ventilation; Diabetic; Elderly; Multiorgan dysfunction

Introduction

Tetanus is caused by tetanospasmin, a potent neurotoxin elaborated by Clostridium tetani, and continues to cause significant morbidity and mortality worldwide (2, 3) despite the availability of effective vaccination. The global burden disproportionately affects elderly, immunocompromised, and unvaccinated populations. Clinical manifestations range from localized muscle rigidity to generalized spasms, trismus (lockjaw), laryngospasm, and life-threatening autonomic dysfunction.

The management of severe tetanus is particularly challenging in patients with pre-existing cardiovascular disease, given the profound haemodynamic instability induced by autonomic dysfunction. To date, few cases have been reported in patients with concurrent restrictive cardiomyopathy and a cardiac implantable electronic device (CIED). This report describes the clinical course and multidisciplinary management of a 70-year-old woman with multiple comorbidities who developed severe generalised tetanus following a penetrating thorn injury, ultimately resulting in a fatal outcome (3, 4).

Case Presentation

Patient Background and Presenting Complaints

A 70-year-old female with a documented history of type 2 diabetes mellitus (DM), restrictive cardiomyopathy (RCM), sinus node dysfunction, and tachy-brady syndrome with symptomatic bradycardia in the context of atrial fibrillation (AFib) presented to our emergency department on 15 March 2026. She had undergone implantation of a VVIR MRI-compatible pacemaker on 22 January 2024.

The patient reported a thorn prick injury to the left hand approximately three days prior, which was initially left untreated. Tetanus toxoid (TT) was administered at an outside facility the following day. On the morning of presentation, she developed progressive dysphagia, dysarthria, and difficulty in mouth opening (trismus). Initial management was commenced at a peripheral facility before she was referred to our centre for further evaluation and intensive care.

Medications on Admission

Her regular medications included: Tab. Safglim VG2(glimepiride, metformin, and voglibose) (1-0-1), Tab. Vildagliptin 50 mg (1-0-1), Tab. Bisoprolol 2.5 mg (1-0-0), Tab. Dytor Plus 5 mg (1-0-0), Tab. Glycin M 40 mg (1-0-0), and Tab. Urvit Gold (1-0-0).

Initial Clinical Examination (15 March 2026)

Vital Signs

Blood Pressure: 140/80 mmHg

Pulse Rate: 84 beats/min

Temperature: 97°F

SpO₂: 99% on room air.

Airway: Patent, no secretions.

Breathing: Spontaneous.

Circulation: Peripheral pulses palpable in all four limbs; skin discolouration noted over left hand and right medial aspect of leg.

Neurological: Moves all four limbs. On examination: temporalis and masseter contraction, platysma contraction, and lockjaw (trismus) positive.

Cardiovascular: S1 and S2 heard. Abdomen soft. Bilateral air entry on auscultation. No stridor or wheeze.

GRBS: 369 mg/dL.

Point-of-Care Ultrasound (POCUS): Adequate left ventricular (LV) function; dilated left atrium (LA), right atrium (RA), and right ventricle (RV); inferior vena cava (IVC) collapsing (50%); bilateral lung A-profile.

Based on these findings, acute-onset lockjaw with a differential of dystonic reaction versus early tetanus was considered. An MRI Brain (stroke protocol) was performed and revealed only age-related cerebral atrophy. Early tetanus was clinically suspected.

Hospital Day 1 – Initial Management (15 March 2026)

Initial empirical management included:

  • Phenergan (Promethazine) 25 mg IM STAT (for suspected dystonic reaction)
  • Tetanus Immunoglobulin (TIG) 3000 IU IM
  • Metronidazole 500 mg IV every 8 hours
  • Diazepam 5 mg IV SOS
  • Intravenous fluids at 60 mL/hr

No significant clinical improvement was observed on re-review later in the day.

Hospital Day 2 – Acute Deterioration and Airway Management (16 March 2026)

At approximately 05:30 hours, the patient developed bilateral upper limb rigidity, jerky movements, and upward deviation of the eyes, followed by bradycardia (HR: 52 beats/min). Bag-mask ventilation was initiated and a nasopharyngeal airway was inserted.

Emergency medications administered:

  • Midazolam 3 mg IV
  • Atropine 1 ampoule IV
  • Levetiracetam (Levepil) 2 g IV in 100 mL normal saline

Post-resuscitation vitals: HR 148 beats/min, SpO₂ 100% (on bag-mask ventilation), BP 130/80 mmHg, GCS E3V2M5. Mouth opening was severely restricted (<2 finger breadths), precluding conventional orotracheal intubation. Anaesthetic and ENT team opinions were urgently sought. Nasopharyngeal intubation was successfully performed. Vitals subsequently stabilised (HR 102 beats/min, SpO₂ 98%, BP 120/80 mmHg). Tracheostomy was planned by the ENT team.

Intravenous antibiotics and ongoing sedoanalgesia were initiated:

  • Ceftriaxone 1 g IV BD (commenced)
  • Levetiracetam 1 g IV BD
  • Human Actrapid infusion 5 U/hr IV (titrated per capillary blood glucose)
  • Fentanyl + Midazolam infusion at 4 mL/hr
  • Benzyl Penicillin 4 million units IV Q6H (one dose given, then withheld)
  • Tetanus Immunoglobulin 2250 IU IM STAT

On review at 09:00, the patient was conscious and obeying commands, afebrile, with generalised spasms. CNS examination: trismus positive, neck rigidity positive, spontaneous limb movements present.

Cardiology opinion was sought due to prior cardiac history. Echocardiography (ECHO) performed on this day revealed: normal LV size and function, mild concentric left ventricular hypertrophy (LVH), mild mitral regurgitation (MR), mild tricuspid regurgitation (TR), and pulmonary arterial hypertension (PAH). Tab. Dytor Plus and Tab. Clopitab CV were prescribed by the cardiology team.

Hospital Day 3 – Ventilatory Support and ID Consultation (17 March 2026)

The patient remained on synchronised intermittent mandatory ventilation (SIMV) with sedation. Recurrent generalised spasms and intermittent hiccups were noted. GCS was E2VETM5. Trismus and drowsiness persisted. Vital signs: BP 140/80 mmHg, HR 108 beats/min, SpO₂ 100%, fasting blood glucose 279 mg/dL.

An Infectious Diseases (ID) physician was consulted. Autonomic dysfunction was confirmed with HR ranging from 68 to 120 beats/min and BP ranging from 90/60 to 160/80 mmHg. Recommendations included:

  • Ensure minimal external stimulation (lights off)
  • Administer TIG 500 IU
  • Continue Metronidazole 500 mg IV every 6 hours for a minimum of 10 days
  • Consider Magnesium Sulphate IV infusion for autonomic dysfunction
  • Initiate active immunisation (Inj. Tdap booster: 3 doses at 0, 1, and 6 months; followed by Td booster every 10 years) once clinically stabilised

Treatment adjustments on this day: Ceftriaxone and Levetiracetam were discontinued. Vecuronium IV infusion (20 mg in 20 mL NS), Lorazepam 4 mg IV STAT, and Diazepam 5 mg IV SOS were added. Fentanyl + Midazolam infusion was increased to 6 mL/hr.

Hospital Day 4 – New Fever and Haemodynamic Instability (18 March 2026)

New-onset fever (temperature 100°F) was noted and tepid sponging was commenced. The patient had been sedated and pharmacologically paralysed overnight. Overnight infusions were stopped in the morning for neurological reassessment. Vital signs: BP 130/70 mmHg, PR 120 beats/min, SpO₂ 99%. Haemoglobin declined from 11.4 to 9.8 g/dL. Fasting blood glucose: 281 mg/dL. GCS off sedation: E1VTM1. Tracheostomy was performed by the ENT team.

Revised diagnosis: Post-traumatic tetanus – acute descending paralysis; shock. Working diagnoses included confirmed tetanus (TIG administered) and haemodynamic instability. Noradrenaline infusion (8 mg in 42 mL NS at 8 mL/hr), Isotonic Bicarbonate (125 mL/hr), and Vecuronium infusion (40 mg in 40 mL NS at 4 mL/hr) were added.

Hospital Day 5 – Post-Tracheostomy, EEG and Metabolic Complications (19 March 2026)

Tracheostomy was confirmed in situ. The patient was placed on SIMV mode via tracheostomy. Haemodynamic monitoring showed: BP 130/70 mmHg, PR 110 beats/min, SpO₂ 100%. Blood ketone level was elevated at 5.5 mmol/L, prompting Human Actrapid infusion. Hypokalaemia (potassium 2.6 mEq/L) was identified and corrected. GCS (under sedation and paralysis): E1VTM1. Fasting blood glucose: 210 mg/dL.

An EEG was performed and reported as: Abnormal EEG suggestive of diffuse cerebral dysfunction. Guarded prognosis was communicated to the patient’s family. Amiodarone 150 mg IV, TIG 500 IU IM, Magnesium Sulphate 2 g IV, and Diazepam 10 mg IV were administered as STAT doses. Clonazepam 0.5 mg (1-0-1) was added to the regular regimen.

Hospital Day 6- Autonomic Instability and Hypernatremia (20 March 2026)

Autonomic instability was prominent: BP fluctuated between 80/40 and 200/113 mmHg. PR 112 beats/min, RR 20 breaths/min, SpO₂ 99%, temperature normal. Decreased neck rigidity and trismus were noted, suggesting partial clinical improvement. Hypernatremia was detected (Na⁺ 153–157 mEq/L). The patient had not passed stools for six days; Dulcolax suppository was administered per rectum with a bowel response.

ENT team review confirmed: Portex tracheostomy tube in situ, cuff inflated, inner cannula in place, no bleeding or oozing. Inner cannula change was recommended twice daily.

DVT prophylaxis was initiated with Inj. Heparin 2500 IU IV BD. Noradrenaline infusion was titrated per blood pressure, and Magnesium Sulphate 4 g in half-normal saline (50 mL/hr) was continued. The patient was transferred from Isolation ICU to the Geriatric ICU.

Hospital Day 7 – Right Foot Wound, Plastic Surgery Consult (21 March 2026)

No fever recorded. Thick tracheal secretions were noted on suctioning. No new jerky movements. BP fluctuations persisted. Erythema and oedema were observed over the dorsum of the right foot the site of the original thorn prick injury. GCS: E1VTM1. Pupils: 1.5 mm bilaterally.

Plastic Surgery consultation was obtained. Local examination revealed an erythematous area over the sole of the right foot (6×6 cm) without warmth. Anterior tibial artery (ATA) and dorsal pedis artery (DPA) were palpable. Inflammatory markers: Procalcitonin 0.91 ng/mL, Total Count 9590/µL.

Ultrasound of the right foot demonstrated dermal thickening over the medial aspect with subcutaneous oedema and an ill-defined hypoechoic collection measuring 24×9 mm in the subcutaneous plane. Insulin infusion was transitioned to a split subcutaneous regimen. Magnesium Sulphate infusion was discontinued.

Hospital Day 8 – Wound Debridement and Serial EEG (22–23 March 2026)

No fever. Thick tracheal secretions. No jerky movements. Haemodynamic instability persisted with BP fluctuations. Noradrenaline was continued and titrated per blood pressure. Bowel management continued with suppository. Human actrapid infusion was stopped; subcutaneous insulin regimen maintained. Fasting blood glucose: 396 mg/dL (23 March). Electrolytes: Na⁺ 146 mEq/L, K⁺ 4.2 mEq/L.

On 23 March 2026, surgical wound debridement of the right foot was performed by the Plastic Surgery team. New blebs were noted on the right upper limb. A repeat EEG again showed: Abnormal EEG report suggestive of diffuse cerebral dysfunction.

Hospital Day 10- Cardiogenic Deterioration (24 March 2026)

Autonomic instability and BP fluctuations persisted. Fasting blood glucose: 299 mg/dL. GCS: E1VTM1 (under sedation). POCUS at this time revealed: moderate LV dysfunction, RA/RV collapse, minimally collapsible IVC, and bilateral minimal basal atelectasis. ABG: pH 7.35, PCO₂ 4.6 kPa, HCO₃ 25.4 mEq/L, Lactate 2.2 mmol/L, K⁺ 3.6 mEq/L, PO₂ 85 mmHg. Na⁺ 149 mEq/L. ECG showed T-wave flattening in leads V4–V6. Troponin I was critically elevated at 2.29 ng/mL (from 0.148 ng/mL on day 2).

Cardiology was urgently consulted. Repeat ECHO demonstrated global severe LV dysfunction, mild MR, and mild TR with PAH, a significant dynamic deterioration from earlier studies. Coronary angiography (CAG) was recommended post-stabilisation. Hydrocortisone 200 mg IV STAT followed by infusion (2 mL/hr) was commenced for suspected adrenal insufficiency. Human Albumin transfusion was planned with consent from the primary team.

At 21:00 hours, the clinical condition worsened dramatically: BP 110/60 mmHg, PR 155 beats/min, RR 26 breaths/min, SpO₂ 96%. Worsening shock prompted initiation of Vasopressin infusion, Magnesium Sulphate 2 g in 100 mL over 1 hour, and Ivabradine 5 mg STAT.

Guarded prognosis was communicated in detail to the patient’s family.

Hospital Day 11 – Cardiopulmonary Arrest and Death (25 March 2026)

At 03:15 hours, the patient developed severe bradycardia with a heart rate below 45 beats/min. Carotid pulse was absent. Advanced Cardiac Life Support (ACLS) protocol was immediately initiated. Inj. Adrenaline 1 mg IV STAT was administered. Return of spontaneous circulation (ROSC) was not achieved. Cardiopulmonary resuscitation (CPR) was continued for 10 minutes, with two doses of Adrenaline administered. ROSC was not obtained despite effective resuscitation.

The patient was declared deceased at 03:39 hours on 25 March 2026.

Certified causes of death:

  • Cardiogenic shock
  • Tetanus with autonomic dysfunction and multiorgan dysfunction syndrome (MODS)
  • Underlying diabetes mellitus and restrictive cardiomyopathy

Summary of Laboratory Investigations

Table 1: Serial laboratory parameters throughout the clinical course.

Parameter15 Mar16 Mar17 Mar19 Mar20 Mar21 Mar22 Mar23 Mar24 Mar
Hemoglobin (g/dL)11.4-9.8---11.8--
PCV (%)35-31.9---37.5--
Total Count (/µL)8980-9590---11810--
Platelets (/µL)29000-228000---159000--
Urea (mg/dL)42----43---
Creatinine (mg/dL)1.0----0.8---
Na⁺ (mEq/L)143--156153150148146149
K⁺ (mEq/L)4.1--3.64.23.84.24.2-
Ca²⁺ (mg/dL)9.5------8.0-
Phosphorus (mg/dL)4.2--------
Mg²⁺ (mEq/L)1.9--------
CPK (U/L)153--------
INR1.19--------
Procalcitonin (ng/mL)--0.91------
Troponin I (ng/mL)-0.148------2.29
Cortisol-R (µg/dL)---61.6-----
Blood Ketone (mmol/L)-0.1-5.5-----

ABG (24 March): pH 7.35, PCO₂ 4.6 kPa, HCO₃ 25.4 mEq/L, Lactate 2.2 mmol/L, PO₂ 85 mmHg. Troponin I rose from 0.148 ng/mL (Day 2) to 2.29 ng/mL (Day 10), indicative of acute myocardial injury. EEG (Days 5 and 9) was abnormal, showing diffuse cerebral dysfunction on both occasions.

Discussion

This case illustrates several critical teaching points in the diagnosis and management of severe generalised tetanus in a medically complex elderly patient (2,3).

Delayed wound care and toxoid administration: Although tetanus toxoid was administered the day following the thorn prick injury, the initial failure to seek timely wound care and the likely inadequate immunisation status (unknown previous vaccination history) allowed sufficient elaboration of tetanospasmin to cause fulminant disease. In immunocompromised individuals and the elderly, even minor penetrating injuries should prompt urgent wound debridement and prophylaxis (1).

Clinical presentation and diagnosis: Trismus, dysphagia, and generalised spasms in the context of a recent penetrating wound represent classic features of generalised tetanus (3). The Ablett classification would place this patient in Grade IV tetanus (2) given the presence of severe autonomic dysfunction, apnoeic episodes, and cardiovascular instability. Dystonic reaction was appropriately excluded early.

Airway management challenges: Trismus precluded conventional orotracheal intubation (mouth opening <2 finger breadths). Early multidisciplinary involvement (Anaesthetics and ENT) facilitated successful nasopharyngeal intubation and timely tracheostomy, which are essential in severe tetanus to secure the airway, facilitate prolonged ventilation, and enable pulmonary toilet (3, 4).

Autonomic dysfunction: Autonomic dysfunction is a hallmark of severe tetanus and a major determinant of mortality (2, 4). In this patient, extreme haemodynamic lability (BP 80/40 to 200/113 mmHg, HR 68 to 155 beats/min) necessitated concurrent use of Noradrenaline, Vasopressin, Magnesium Sulphate (as an autonomic modulator), and Ivabradine (4). The co-existence of restrictive cardiomyopathy and pacemaker dependency further complicated haemodynamic management, as standard vasopressor titration was challenging in the setting of fixed cardiac output physiology.

Cardiovascular deterioration: The marked rise in Troponin I (0.148 to 2.29 ng/mL) and acute deterioration in LV function (from preserved to severe global dysfunction on ECHO) suggest tetanus-associated cardiomyopathy or acute stress-related myocardial injury superimposed on the pre-existing restrictive cardiomyopathy (3, 4). The dynamic haemodynamic changes from autonomic surges, combined with underlying structural cardiac disease, created an irrecoverable cardiogenic state.

Metabolic and infective complications: Poorly controlled diabetes (glucose 210–396 mg/dL) contributed to immunosuppression, delayed healing of the wound, and ketosis. Persistent hypernatremia (Na⁺ up to 157 mEq/L), hypokalaemia, and rising inflammatory markers reflected the severity of systemic illness (2). Serial EEG demonstrating diffuse cerebral dysfunction corroborated the degree of neurological compromise.

Pacemaker and tetanus: The VVIR pacemaker complicated the management of tetanus-induced bradyarrhythmias. Pacemaker-mediated rhythm prevented recognition of intrinsic bradycardia at earlier stages, while autonomic surges caused competing tachyarrhythmias. This combination underscores the unique management challenge posed by CIEDs in tetanus patients with autonomic dysfunction (3).

Conclusion

This case highlights the devastating potential of tetanus in elderly patients with multiple comorbidities, particularly pre-existing cardiomyopathy, diabetes mellitus, and cardiac implantable electronic devices. Despite prompt multi-disciplinary management — including tetanus immunoglobulin, metronidazole, tracheostomy, mechanical ventilation, pharmacological paralysis, sedoanalgesia, and haemodynamic support — the patient’s severe autonomic dysfunction and cardiogenic deterioration led to a fatal outcome.

This report reinforces the critical importance of: (1) universal tetanus vaccination and booster adherence, particularly in elderly and immunocompromised individuals; (2) meticulous wound care following any penetrating injury; and (3) early specialist involvement in the management of severe tetanus with cardiovascular comorbidities. A low threshold for tetanus prophylaxis must be maintained for all wound presentations, regardless of perceived severity.

Role of the Clinical Pharmacist:  The clinical pharmacist holds a pivotal role in the management of a case of this complexity. In the acute care setting, this encompasses proactive drug interaction screening — particularly the QT-prolonging risk of concurrent Amiodarone and Ivabradine, the potentiation of neuromuscular blockade by Magnesium Sulphate, and the heightened bleeding risk from simultaneous antiplatelet and anticoagulant therapy in a patient with fresh surgical wounds. Ongoing therapeutic monitoring responsibilities include insulin infusion titration against capillary blood glucose, recognition of impaired subcutaneous insulin absorption during vasopressor therapy, daily sodium load auditing across all intravenous preparations to detect and prevent drug-induced hypernatraemia, and ensuring adequate sedation depth is maintained whenever neuromuscular blocking agents are in use. At the preventive level, embedding routine immunisation status review into pharmacy-led medication reconciliation during chronic disease follow-up represents the most impactful intervention of all — one that, had it been applied in this case, may have averted the admission entirely.

References

  • Liang JL, Tiwari T, Moro P, Messonnier NE, Reingold A, Sawyer M, et al. Prevention of pertussis, tetanus, and diphtheria with vaccines in the United States: recommendations of the Advisory Committee on Immunization Practices. MMWR Recomm Rep. 2018;67(2):1-44.
  • Farrar JJ, Yen LM, Cook T, Fairweather N, Binh N, Parry J, et al. Tetanus. J Neurol Neurosurg Psychiatry. 2000;69(3):292-301.
  • Cook TM, Protheroe RT, Handel JM. Tetanus: a review of the literature. Br J Anaesth. 2001;87(3):477-87.
  • Rodrigo C, Fernando D, Rajapakse S. Pharmacological management of tetanus: an evidence-based review. Crit Care. 2014;18(2):217.
  • Thwaites CL, Beeching NJ, Newton CR. Maternal and neonatal tetanus. Lancet. 2015;385(9965):362-70.

 

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