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Diagnosis & Treatment — General practitioner / health post

 

General problems

At particular risk are: children, elderly people, patients with pre-existing conditions, such as coronary heart disease, arterial hypertension, lung disease, kidney disease, allergies (sensitisation), patients with predilection sites for bleeding such as gastrointestinal ulcers, kidney stones, pulmonary cavities (tuberculous), and patients taking particular drugs, such as coumarin derivatives, platelet aggregation inhibitors and beta-blockers.

Patient presents with a tourniquet on the affected extremity

D  Diagnostics

Check venous and arterial blood supply in the extremity.

C  Comments

If a tourniquet has been applied, it should not be removed until antivenom is at hand or has been administered and the means for treating complications, including possible complications caused by the antivenom, are available.

If these requirements cannot be met within a suitable period of time, it is necessary to weigh the risk of the systemic effects of the venom that could occur after removing the tourniquet against the risk of progressive local tissue damage that may arise if the bandage is left in place.

The development of severe signs of envenoming within minutes after removal of a tourniquet has been described (Pearn et al. 1981).

Is it likely that a clinically relevant injection of venom has taken place?

D  Diagnostics

Inquire re:

  • time of the bite,
  • local pain,
  • headache, nausea, vomiting,
  • abdominal pain,
  • muscle pain.

Assess:

  • state of consciousness.

Measure:

  • blood pressure/pulse,
  • respiratory rate.

Observe/investigate:

  • bite marks,
  • extent and intensity of local swelling,
  • enlargement and painfulness of regional lymph nodes,
  • clinical signs of shock,
  • bleeding in the region of the swelling,
  • bleeding from bite marks and other injuries,
  • gingival bleeding,
  • blood-stained sputum, vomit ("coffee ground vomitus"), stools (melaena) or urine,
  • acute abdomen (intra-abdominal bleeding!),
  • focal neurological deficits, meningismus (intracranial bleeding!),
  • cranial nerve deficits, such as ptosis, ophthalmoplegia, dysphagia, dysarthria,
  • paralysis of the skeletal musculature including the respiratory musculature (→ respiratory insufficiency/respiratory failure),
  • myalgia with active and passive movement and upon pressure, pseudotrismus,
  • dark-brown/red urine (differential diagnosis haemoglobinuria) (rhabdomyolysis!),
  • flank pain and renal bed sensitive to percussion.

Determine:

C  Comments

The symptoms and degree of envenoming depend not only on the amount of venom injected and numerous other variables, but also on the time that has elapsed since the bite. This variable factor must be taken into account when making the following decisions:

  • exclusion of envenoming (see below),
  • the time interval between clinical examinations (see Therapy phase: Hospital),
  • emergency care (see below).

The fact that a patient has been bitten by a known venomous snake and the presence of bite marks do not automatically allow the conclusion that a clinically significant injection of venom has taken place.

With many Australian elapids, local signs, such as pain and swelling at the site of the bite, are not a reliable indicator that injection of venom has taken place.

With Pseudonaja sp. bites there are generally no local signs at all. Cases of Australian elapid bites that have occurred unnoticed have been described, especially in children. Only when the children showed signs of systemic envenoming was a snakebite considered as the differential diagnosis. Detection of venom antigen in the serum and urine or venom residue from the region of the bite confirmed the diagnosis (Gaynor et al. 1977, White et al. 1983–84).

If a significant amount of venom is injected during a bite from an Australian elapid, painful enlargement of regional lymph nodes frequently occurs as a sign of systemic envenoming.

Australian elapids cause early (autopharmacological) symptoms of envenoming, nausea, vomiting, abdominal pain, collapse etc., which represent a reliable indication of systemic envenoming.

Noticeable bleeding is generally absent, even if defibrin(ogen)ation is present to such a degree that the blood is completely incoagulable (clotting time test). For this reason the simple clotting time test should always be performed if a snakebite is suspected. However, not all Australian elapids cause haemostatic defects.

Paralysis and clinical as well as laboratory signs of myolysis are reliable indicators of a systemic effect of the venom; however, again it is the case that not all Australian elapids cause such effects.

A validated immunological test kit is available for Australian elapids (CSL, Parkville, Australia). This kit can be used not only for indirect species identification and thus to choose the appropriate antivenom but also to estimate circulating venom in the serum and eliminated venom in the urine (Sutherland 1992, Sutherland and King 1991). Cross-reactions do occur.

Exclusion of clinically relevant envenoming

D  Diagnostics

Monitoring for signs and symptoms (see above) that would indicate systemic envenoming for at least 24 h (Sutherland and King 1991, White 1987b) (for recommended examinations, see Therapy phase: Hospital).

Preclinical phase of severe autopharmacological effects (collapse): 15 min (median) (Oxyuranus sp.) (Currie et al. 1992b).

Preparalytic phase: 390 min (median) (Oxyuranus sp.) (Currie et al. 1992b).
Preclinical phase of a haemostatic defect (bleeding): 105 min (Oxyuranus sp.) (Currie et al. 1992b).
Even severe haemostatic defects that can be detected on laboratory tests may not become clinically evident for a long period, or even not at all.

C  Comments

A study of over 110 symptomatic Oxyuranus scutellatus canni bites provides information on the preclinical phase of significant effects of envenoming (Currie et al. 1992a).

Who requires antivenom?

D  Diagnostics

Antivenom indications (overview)
Systemic signs of envenoming:

  • arterial hypotension,
  • haemostatic defects (clinically, laboratory parameters: clotting time or more complex tests),
  • ptosis, ophthalmoplegia, dysphagia, dysarthria,
  • paralysis of the limb musculature,
  • paralysis of the respiratory musculature (→ respiratory insufficiency/failure),
  • myalgia with active and passive movement,
  • myoglobinuria (dark, brown/black or red urine),
  • elevated CPK, GOT (AST),
  • acute renal failure.

How is the appropriate antivenom chosen?

D  Diagnostics

How are antivenoms administered and complications caused by antivenoms treated?

T  Treatment
C  Comments

Symptomatic emergency medical treatment and antivenom treatment are complementary strategies.

The aim of antivenom treatment is neutralisation of the venom. The success of antivenom treatment depends on the quality of the antivenom, the specific properties of those venom components relevant to envenoming and the time point at which antivenom is administered.

Symptomatic emergency medical treatment
1. Clinical signs of shock

S  Signs & Symptoms

Early: anaphylactic/anaphylactoid shock.

T  Treatment
  • Treatment of the anaphylactic/anaphylactoid shock,
  • possibly antivenom.
S  Signs & Symptoms

Late (hours to days after the bite): haemorrhagic shock.

T  Treatment
  • Treatment of the haemorrhagic shock,
  • antivenom.

Symptomatic emergency medical treatment
2. Clinical signs of progressive paralysis; paralysis of the respiratory musculature (→ dyspnoea, respiratory failure)

T  Treatment
C  Comments

The efficacy of acetylcholinesterase inhibitors has only been demonstrated for Australian elapid bites with an exclusively postsynaptic neurotoxic venom effect (Acanthophis sp.) (Currie et al. 1988, 1990, Hudson 1988).

Symptomatic emergency medical treatment
3. Clinical signs of focal neurological deficits, meningismus (intracranial bleeding!)

T  Treatment
  • Treatment of the intracranial bleeding,
  • antivenom.

Symptomatic emergency medical treatment

4. Clinical signs of acute renal insufficiency

T  Treatment
  • Treatment of the acute renal insufficiency,
  • antivenom.

Local treatment

Bite wound, including the surrounding reaction

D  Diagnostics
  • Assessment of the wound according to the usual criteria.
  • Swelling: assessment of the extent and increase in magnitude; regional signs of haemorrhage.
  • Long-term: observation for the formation of necrosis.
T  Treatment
  • Cleaning, disinfection and dressing of the wound at regular intervals.
  • Immobilisation of the extremity with a splint. Padding and monitoring to prevent pressure necrosis and disturbance of the blood circulation if the oedema increases.
  • Possibly also prophylactic antibiotic treatment:
    • no interference with the bite wound: penicillin or erythromycin,
    • bite wound has been interfered with (incisions etc.): penicillin or erythromycin + aminoglycoside (Warrell 1990b).
C  Comments

As Australian elapid bites generally do not cause any marked local symptoms of envenoming (exception: Pseudechis australis), local complications are extremely uncommon.

Tetanus

T  Treatment

Tetanus prophylaxis.