Tetanus And Gas Gangrene Treatment And Diagnosis Notes

Tetanus And Gas Gangrene Tetanus

Tetanus Introduction

1. A nonimmunised, 18-year-old girl was admitted with moderate tetanus following a nail prick in her foot. In the hospital, she developed convulsions, laryngeal oedema, and cardiac arrest. She was resuscitated and shifted to the intensive care unit under an anaesthesiologist’s care.
2. Tracheostomy, ventilation, and paralysing agents were used. Unlike many others, she was lucky. She walked home after two months of stay in the intensive care unit after a lot of suffering and spending a lot of money.
3. This happened in the early 90s. Due to extensive immunisation programmes in the last few decades, tetanus has become a rare disease in India. Case history has been presented here to allow students to reflect on the following:

Read And Learn More: General Surgery Notes

• • How important is immunisation to prevent tetanus?
  • How serious is this disorder?
  • Is it possible to save these patients if they are critically ill?

Tetanus Definition

Tetanus is a serious disorder caused by the toxin of the Clostridium tetani affecting the nervous system and gives rise to muscle contraction of the neck, back and jaw muscles. It is popularly called lockjaw.

Tetanus Aetiopathogenesis

• It is caused by Clostridium tetani, an anaerobic sporeforming bacillus with terminal spores that have a drumstick-like appearance.
• Narcotic addicts who inject themselves beneath the skin at many sites are vulnerable—‘Skin Poppers’.

Tetanus Possible Routes Of Infection

• Umbilical cord (in neonates)—seen in communities that practise cow dung application on the umbilical stump.
• Wound, as a complication of road traffic accidents where other aerobic organisms reduce oxygen tension in the wound, thereby facilitating the growth of anaerobic Clostridium tetani.
• Wounds which are more Prone to Tetanus
  • Time—wound more than 6 hours old
  • Extensive contamination by soil, faeces, rust
  • Tissue devitalised or denervated
  • Animal or human bites
  • No less than 1 cm (more than 1 cm)
  • Ulcer or wound—deeper
  • Stellate wounds—burst type
  • Remember as TETANUS
• Minor injuries with rusted nails, ear piercings, tattooing, injections, etc.
• Endogenous infection after septic abortion or surgical operations on the gastrointestinal tract.
• Tetanus due to infection acquired in the operation theatre.
• Thus, tetanus is a wound infection. “No wound, no tetanus” is true. Having entered the wound, the organisms multiply and produce powerful exotoxins which produce the disease. Thus, the organisms by themselves do not produce the disease. The toxins produced by the organisms are tetanospasmin (neurotoxin) and tetanolysin (haemolysin).
• Tetanospasmin has an affinity towards nervous tissues. It reaches the central nervous system along the axons of motor nerve trunks. The toxin gets fixed to the motor cells of the anterior horn cells. The toxin, which is fixed to the motor end plate, acts in the following ways:
  1. It inhibits the release of cholinesterase, leading to the accumulation of acetylcholine at the motor end plate. This causes tonic rigidity of limb, trunk, abdominal, and neck muscles.
  2. It acts at the spinal level and causes reflex muscle contraction due to minor stimuli.
• The toxin, once fixed to the nervous tissue, cannot be neutralised. However, circulating toxins may be neutralised. The incubation period varies from a few days to months or years and is not important.
• The interval between the first symptom (dysphagia and stiffness of the jaw) and the reflex spasm is called the period of onset. If this is less than 48 hours, the prognosis is poor, whereas if it is more than 48 hours, the prognosis is better.
• Tetanolysin also contributes to the pathogenesis of tetanus, but its action is not clear. It is a type of protein which is oxygen-sensitive haemolysin.

Favourable Conditions for the Development of Tetanus

• No immunisation
• Foreign body
• Injury
• Improper sterilisation
• Devitalised tissues
• Anaerobic conditions

Special Types Of Tetanus

1. Tetanus neonatorum: It occurs due to contamination of the umbilical cord in children born to nonimmunised mothers. It usually manifests around 6–8 days of birth and is called eighth-day disease. It carries almost 100% mortality.

2. Local tetanus: In this, muscle contraction occurs in the neighbourhood of the wound.

3. Cephalic tetanus: Usually occurs after a wound over the head and or face. Cranial nerves, such as the facial and oculomotor nerves, may get paralysed. It carries a poor prognosis.

4. Bulbar tetanus: It involves the muscles of deglutition and respiration and is fatal.

5. Latent tetanus: It develops after a few months to years following a wound that might have been forgotten.

6. Puerperal tetanus: It occurs as a complication of abortion or puerperal sepsis.

7. Postoperative tetanus: It occurs due to improper sterilisation of instruments and carries 100% mortality. This type of tetanus should not occur in a modern operation theatre.

8. Otitis tetanus: It is due to chronic suppurative otitis media. In these cases, the wound is a tear in the tympanic membrane. It may occur in any age group but is more common in children and young adults.

Special Types Of Tetanus Clinical Features

• Autonomic dysfunction: Increased basal sympathetic tone, manifesting as tachycardia, bladder or bowel dysfunction, labile hypertension, pyrexia, pallor, sweating, and cyanosis of the digits.
• Episodes of bradycardia, low central venous pressure, and even cardiac arrest have been reported due to parasympathetic dysfunction.
• Complications include pneumonia, urinary tract infection, etc.

Clinical features with differential diagnosis

 

Treatment Of Established Tetanus

1. General management
2. Specific management

1. General Management

• Admission and isolation in a quiet room, to avoid even minor stimuli that may precipitate spasm.
• Wound care—drainage of pus, excision of necrotic tissue, removal of any foreign body, and proper dressing. Exudate or pus may demonstrate gram-positive rods.
• Inj. Tetanus toxoid 0.5 ml intramuscularly (IM).
• Antitetanus serum (ATS) is 50,000 units IM and 50,000 units slow intravenously (IV). This should be given only after giving a small subcutaneous test dose of serum diluted with ten times saline. It has become less popular due to the availability of human antitetanus globulin.
• Human antitetanus globulin 3000–4000 units intramuscular. It is better and safer than ATS, does not cause anaphylaxis, and does not require a test dose.
• Inj. crystalline penicillin 10 lakh units IM 6th hourly is the drug of choice against Clostridium tetani. It may have to be given for 7–10 days.
• Metronidazole 500 mg IV 8th hourly for 10 days. It is more effective than penicillin.
• After recovery, full immunisation with tetanus toxoid is required.

 

2. Specific Management

Specific Management Mild Cases

• There is only tonic rigidity without spasm or dysphagia. These patients are managed by heavy sedation with a combination of drugs to prevent spasms or convulsions. The treatment method followed in our hospital is given.
• Benzodiazepines and morphine act centrally to minimise the effects of tetanospasmin.
• Chlorpromazine, an α-receptor blocker, may decrease sympathetic activity. Other α-blockers like phenoxybenzamine and phentolamine have also been used.
• These drugs are repeated in such a way that the patient receives some sedative every two hours. The dosage of the drugs is adjusted once every 2 or 3 days to get the maximum effect of sedation or muscle relaxation.
• Injection of diazepam 10 mg, a tracheostomy set, and a resuscitation set with a laryngoscope and endotracheal tubes should be kept ready by the side of the patient.
• When a high dose of diazepam is used, it can give rise to hyper-osmolarity and metabolic acidosis because of propylene glycol (vehicle). Midazolam is better.
• Labetalol has both alfa and beta-blocking properties. It also can be used. Dose is: 0.25 mg to 1 mg/mt.

Method Of Treatment

 

Specific Management Seriously 3 Cases

• They have dysphagia and reflex spasms.
• A nasogastric tube is introduced for feeding purposes and to administer the drugs.
• Tracheostomy, if breathing difficulty arises.

Specific Management Dangerously 3 Cases

This group includes patients with major cyanotic convulsions. In addition to continuing sedatives, these patients are paralysed with muscle relaxants (neuromuscular blocking agents) and are mechanically ventilated till they recover.

• The duration of required ventilatory support cannot be predicted. During this period, supportive therapy, such as adequate nutrition, bladder and bowel care, and frequent change of position to avoid bedsores, is required.
• Magnesium sulphate may be used to treat autonomic complications and control spasms. It may be used alone or in combination with benzodiazepines. A loading dose of 5 g over 20 min is followed by an infusion.
• The rate of which is titrated to control spasms as well as reduce muscle rigidity to a level acceptable by the patient for swallowing saliva, mouth care, and limb physiotherapy. Total abolition of muscle rigidity is not required and may lead to hypotonia.
• Loss of patellar reflex may not be a valid indicator of hypermagnesaemia in all patients, as the reflex is sometimes masked by rigidity and tends to be lost early in elderly patients. The patients, therefore, should be monitored closely for ventilatory depression.
• Magnesium sulphate may not reduce the need for mechanical ventilation in patients with severe tetanus but may help in reducing the requirement for other sedatives.

Prophylaxis

1. Tetanus neonatorum may be prevented by administering two tetanus toxoid injections, 0.5 ml IM, to the mother in the second trimester of pregnancy.

2. Infants and children are immunised with tetanus toxoid, diphtheria, and pertussis vaccine (DPT–triple antigen) at 6, 10, and 14 weeks of age, with a booster dose at 18 months 5 years, followed by 0.5 ml tetanus toxoid once every five years.

3. Immunised individuals who receive a provocative injury are administered a booster dose if they have not received one in the previous 5 years. Tetanus may be prevented by giving tetanus antitoxin in the following situations:

Wounds of the head and or face, penetrating wounds, wounds with contused and devitalised tissues war wounds and road traffic accidents. 1,500 IU of antitoxin should be given subcutaneously or intramuscularly as early as possible. Treatment of the wound is done. In severe wounds, the dose may be doubled.

Complications: Most of these may also be the causes of death.

1. Aspiration of pharyngeal contents into the lungs results in aspiration pneumonia.
2. Laryngeal spasm and respiratory arrest, resulting in cardiac arrest.
3. Autonomic disturbances, resulting in cardiac arrhythmias: In some patients, pacemaker insertion may help if there is refractory bradycardia.

A Case Report Of Neck Rigidity

• A 48-year-old lady who had undergone vaginal hysterectomy 10 days prior was brought to our hospital as a case of ‘tetanus.’ On examination, she had neck rigidity and
  difficulty in mouth opening. Abdominal rigidity was mild.
• She appeared pale. Pallor was attributed to anaemia caused by ‘dysfunctional uterine bleeding’ (DUB), for which she was operated. She was diagnosed with postoperative tetanus and was started on treatment.
• The next day, she was unresponsive to commands. Laboratory reports, which had been sent the previous day, showed a total WBC count of 44,000 cells/mm3 clinching the diagnosis of ‘leukaemia.’ Neck rigidity was due to leukaemic infiltrates in the meninges. Now you know the cause of uterine bleeding!!!

Gas Gangrene

Gas Gangrene Definition:

• It is a highly fatal, rapidly spreading infection caused by clostridial organisms that result in myonecrosis.
• Gas produced by organisms consists of predominantly nitrogen, and others are hydrogen, carbon dioxide and oxygen. (E. coli, Klebsiella, Proteus, Candida, Bacteroides, and Peptostreptococcus are a few other gas-forming organisms.)
• Other names for gas gangrene are clostridial myositis, clostridial myonecrosis, and infective gangrene of the muscles.

Gas Gangrene Aetiology

The disease is most commonly (60%) caused by Clostridium perfringens (Clostridium welchii). Other organisms include Clostridium septicum, Clostridium oedematiens, and Clostridium histolyticum. These are gram-positive, anaerobic, spore-forming bacilli.

Gas Gangrene MacLennan Anaerobic Wound Infection Types

1. Simple wound contamination—no invasion of the underlying tissue
2. Anaerobic cellulitis—invades fascial planes with minimal toxins in muscles
3. Anaerobic myositis—muscle necrosis

Gas Gangrene Sources of Infection and Predisposing Factors

Predisposing factors for the development of gas gangrene

 

Manured soil or cultivated soil, normal intestines.

Types Of Gas Gangrene Infections

1. Clostridial cellulitis: In this condition, healthy muscles are not involved. It involves necrotic tissues and produces features of cellulitis such as tense, swollen parts with palpable crepitus. However, it is a mild infection and may be managed conservatively with antibiotics.
2. Local type: It refers to infection confined to a single muscle.
3. Group type: It refers to infection confined to a group of muscles in a single compartment. Such cases benefit from a compartmental excision.
4. Massive type: Gas gangrene involving the entire limb and requiring amputation.

 

Gas Gangrene Risk Groups

• Patients who have had lower limb amputations performed for ischaemic gangrene (may develop infection from their own bowel organisms).
• High-velocity gunshot wounds with perforation of a hollow viscus (military wounds).
• Immunocompromised patients.
• Trauma is postoperative—the most common form of gas gangrene (70%).
• Patients with diabetes mellitus, blood vessel disease (atherosclerosis), or colon cancer.
• Intravenous drug users and gas gangrene: Repeated trauma of the needle due to intramuscular pr deep injections, and anaerobic environment facilitates the development of gas gangrene in these patients. Clostridia can survive in heroin preparations.

Risk Groups Pathogenesis

• Gas gangrene develops in wounds that are heavily contaminated with soil or a foreign body, or in those associated with a laceration and devitalised muscle mass. This type of situation is common following road traffic accidents.
• Endogenous infection from the patient’s faecal matter may be responsible for gas gangrene in certain cases of contamination of a surgical wound caused by below-knee amputation done for some other cause.
• All these factors contribute to creating low oxygen tension. Under these favourable conditions, clostridial organisms multiply and produce toxins that cause further tissue damage.
• Once powerful toxins start acting, various pathological events, such as inflammation, oedema, muscle necrosis, and gangrene of the muscles, set.
• Features of SIRS (systemic inflammatory response syndrome) are present.
• Why does Gas Gangrene spread fast?
  • Massive infection
  • Gross injury
  • Devitalised tissue
  • Poor immunity
  • Foreign body

Risk Groups Clinical Features

• Severe pain in the limb, swelling, fever, and toxicity.
• In untreated cases, the necrotic process continues and septicaemia, renal failure, peripheral circulatory failure, and death occur. The foamy liver is a condition wherein gas is produced in the liver as a part of septicaemia.

Risk Groups Systemic Complications

• Liver necrosis—jaundice
• Haemolytic anaemia
• Renal failure

Diagnosis

• In addition to clinical suspicion, an easy method of confirming the diagnosis is to examine the pus under microscopy after Giemsa staining.
• These organisms are gram-positive and spore-bearing.
• Lecithinase test or Nagler’s reaction: Many species of Clostridium produce lecithinase (C. baratti, C. absonum, C. bifermantans, C. sordelli, and C. novyi). However, the alpha (α) toxin of C. perfringens has phospholipase activity. It neutralises the Lecithin C activity which forms the basis for Nagler’s reaction.
• X-rays, computerized tomography (CT) scans and magnetic resonance imaging (MRI) scans: These will reveal gas and the extent of tissue damage. A few differences between clostridial myonecrosis and non-clostridial necrotising infections are given.

Differences between clostridial myonecrosis and non-clostridial necrotising infections

Diagnosis Prophylaxis

As gas gangrene is highly fatal, it is better to prevent its development by observing the following principles during wound management:

1. Debridement: All dead muscles, necrotic tissues, bone pieces, and foreign material should be removed. Pus should be evacuated. The wound should be thoroughly irrigated with antiseptic agents.
2. Prophylactic antibiotics: Penicillin is the drug of choice. Injection crystalline penicillin 10–20 lakh units 4–6th hourly should be given for 7 days.
3. Judicious and minimal use of tourniquets: If possible, tourniquets should be avoided while managing such a wound in the leg.
4. Gentle but effective application of a plaster cast with or without treatment of associated fractures to avoid compressing the blood vessel.

Diagnosis Treatment Of Established Gas Gangrene

Summary of Gas Gangrene

• • Correct hypotension
  • Control infection
  • Treat dehydration
  • Early debridement
  • Administer hyperbaric oxygen
  • Give blood transfusion
  • Passive immunisation
  • To save lives, amputate

Diagnosis Principles Of The Treatment

The triad of gas gangrene treatment principles are Antibiotics, debridement and hyperbaric oxygen therapy. Other treatment includes supportive treatment.

1. Antibiotics should be continued: Injection of crystalline penicillin 10–20 lakh units 4–6th hourly should be given for 7 days. Systemic Inflammatory Response Syndrome (SIRS) can be caused by Clostridium septicum. It is treated by clindamycin 600–900 mg 8th hourly, vancomycin 1 g 12th hourly, or metronidazole 500 mg 8th hourly.

2. Surgery: Emergency surgery with excision of all dead muscles and necrotic tissues by using generous, long incisions. This is called debridement. This is the most important part of the treatment. However, when the patient is severely ill with hypotension and shock, the only life-saving measure is amputation.

3. Hyperbaric oxygen therapy: It will reduce the amount of toxins produced by the organisms. The patient is asked to lie down in a chamber and pressure inside the chamber will slowly rise to about 2.5 times the normal atmospheric pressure.

Diagnosis Supportive Treatment

• Blood transfusions before, during and after surgery.
• Polyvalent anti-gas gangrene serum.

Diagnosis clinical notes

• A 40-year-old gentleman presented to the hospital with massive gas gangrene involving his right upper limb, chest wall, abdominal wall, and back. It started after an injury to his right elbow. The patient had initially received treatment at a local hospital.
• Due to a lack of proper facilities, he was neither subjected to any surgical procedure nor given any resuscitation. When he came to our hospital, he was in septic shock. It was too late when we saw the patient.
• He had severe hypotension and renal failure. Emergency resuscitation and debridement were done. However, within six hours of admission, he expired.