1
Q
How common are snake bites in South Africa?
A
Snake bites are common in South Africa and represent a significant medical emergency.
2
Q
What is the incidence of snakebite hospital admissions in South Africa?
A
Approximately 30–80 hospital admissions per 100,000 population per year.
3
Q
How many venomous snake species are found in South Africa?
A
About 35 venomous species.
4
Q
How many South African snakes are potentially fatal to humans?
A
Only ~10 species are considered potentially fatal.
5
Q
What is the key reassuring fact about snake bites in South Africa?
A
Most venomous snakes are not lethal, and many bites are dry bites or cause mild envenomation.
6
Q
What are the three main groups of venomous snakes in South Africa?
A
Elapidae
Viperidae
Back-fanged snakes
7
Q
Which snakes belong to the Elapidae family?
A
Cobras and mambas
8
Q
What type of venom do Elapidae snakes typically have?
A
Neurotoxic venom → causes paralysis and respiratory failure.
9
Q
Which snakes belong to the Viperidae family?
A
Adders and vipers (e.g. puff adder)
10
Q
What type of venom do Viperidae snakes typically have?
A
Cytotoxic and haemotoxic venom → tissue necrosis, swelling, bleeding.
11
Q
Which snakes are classified as back-fanged in South Africa?
A
Boomslang and vine snakes
12
Q
What type of venom is characteristic of back-fanged snakes?
A
Haemotoxic venom, especially severe with boomslang bites.
13
Q
Which back-fanged snake is most dangerous in South Africa?
A
Boomslang — causes severe coagulopathy and bleeding.
14
Q
What are the three main types of snake venom?
A
Neurotoxic
Cytotoxic
Hemotoxic
15
Q
Where does neurotoxic venom act?
A
At the synaptic cleft of the neuromuscular junction.
16
Q
Which snakes mainly produce neurotoxic venom in South Africa?
A
Black mamba
Non-spitting cobras
Small adders
17
Q
How does black mamba venom act?
A
Causes increased acetylcholine levels, leading to neuromuscular dysfunction.
18
Q
How does non-spitting cobra venom act?
A
Contains post-synaptic neurotoxins, similar to curare, blocking acetylcholine receptors.
19
Q
Which small adders have neurotoxic venom?
A
Berg adder
Peringuey’s adder
Desert adders
20
Q
What is the mechanism of neurotoxic venom in small adders?
A
Pre-synaptic toxins → inhibit acetylcholine release
21
Q
What is the primary effect of cytotoxic venom?
A
Direct tissue injury and necrosis.
22
Q
What enzymes are found in cytotoxic venom?
A
Proteolytic enzymes.
23
Q
What is the role of hyaluronidase in cytotoxic venom?
A
Facilitates tissue spread of other toxins.
24
Q
Which snakes are classically associated with cytotoxic venom?
A
Puff adder
Gaboon viper
25
Which snakes produce hemotoxic venom?
Back-fanged snakes – mainly boomslang and vine snake.
26
Which clotting factors are activated by hemotoxic venom?
Factor II (prothrombin) and Factor X.
27
What coagulation disorder is caused by hemotoxic venom?
Consumption coagulopathy.
28
When does bleeding typically occur after hemotoxic envenomation?
6–24 hours post-bite.
29
What is the major life-threatening complication of hemotoxic venom?
Disseminated intravascular coagulation (DIC) → multiple organ failure.
30
Should identification of the snake be attempted?
No. Snake identification is often inaccurate and not recommended.
31
Why is snake identification discouraged at the scene?
It increases the risk of other people being bitten.
32
Does a snake bite always result in envenomation?
No. Envenomation may not occur (dry bite).
33
What proportion of snakebite victims never see the snake?
About 40%.
34
What is the recommended approach to snakebite management?
A syndromic approach — treat based on clinical presentation, not snake species.
35
What are the three major snakebite syndromes?
Progressive Pain and Swelling (PPS)
Progressive Weakness (PW)
Bleeding (B)
36
What does Progressive Pain and Swelling (PPS) suggest?
Cytotoxic envenomation → local tissue injury and edema.
37
What does Progressive Weakness (PW) suggest?
Neurotoxic envenomation → neuromuscular paralysis.
38
What does Bleeding (B) suggest?
Hemotoxic envenomation → coagulopathy and hemorrhage.
39
Can snakebite syndromes overlap?
Yes. Patients may present with combinations of PPS, PW, and B.
40
Why is the syndromic approach important?
It guides early management and antivenom use even when the snake is unknown.
41
Which snakes commonly cause Progressive Pain and Swelling (PPS)?
Adders and spitting cobras.
42
What type of envenomation causes PPS?
Cytotoxic envenomation.
43
What proportion of envenomations in South Africa present as PPS?
About 90%.
44
What are the key local features of PPS?
Severe local pain, extensive swelling, and blister formation.
45
How does the swelling in PPS feel on examination?
Painful, tender, warm to hot, and indurated.
46
When does swelling typically begin in PPS?
Within minutes at the site of the bite.
47
How does the swelling spread in PPS?
Spreads proximally, rapid early, then slower later.
48
What serious local complications can occur in PPS?
Compartment syndrome and tissue necrosis.
49
What determines the rate of swelling spread in PPS?
Mainly species-dependent.
50
What type of venom causes Progressive Weakness (PW)?
Neurotoxic venom.
51
Which snakes most commonly cause PW in South Africa?
Mambas and non-spitting cobras.
52
How common is PW compared to PPS?
Less common, but potentially fatal.
53
Why is PW life-threatening?
Causes progressive respiratory muscle paralysis → respiratory failure.
54
What is the characteristic pattern of paralysis in PW?
Progressive descending flaccid paralysis.
55
What early sensory symptoms may occur in PW?
Transient paraesthesia of the tongue and lips.
56
What ocular signs are seen in PW?
Blurred vision, diplopia, ptosis, and dilated pupils.
57
Which cranial nerves are commonly affected in PW?
Facial muscles and other cranial nerves → facial weakness.
58
What bulbar symptoms suggest PW?
Dysphagia and increased oropharyngeal secretions
59
What respiratory features indicate severe PW?
Respiratory distress progressing to respiratory failure.
60
Which systemic features may accompany PW?
Anosmia, complete ophthalmoplegia, and hyponatremia.
61
What is the most important immediate treatment in PW?
Early ventilatory support.
62
What antivenom is used for PW in South Africa?
Polyvalent antivenom.
63
Does antivenom reverse established paralysis?
No — it prevents progression, hence early administration is critical.
64
What venom type causes the Bleeding syndrome?
Hemotoxic venom.
65
Which snakes commonly cause bleeding syndrome in South Africa?
Boomslang
Vine snake
Puff adder
Gaboon viper
66
What is the hallmark laboratory feature of this syndrome?
Incoagulable blood due to consumption coagulopathy.
67
What early, non-specific symptoms may precede bleeding?
GI upset, headache, dizziness, and fainting.
68
What is an early local bleeding sign after the bite?
Oozing of blood from fang punctures or other wound sites.
69
When does bleeding typically start after envenomation?
6–24 hours post-bite.
70
When do late systemic haemostatic manifestations occur?
>24 hours to several days after the bite.
71
What mucocutaneous bleeding manifestations are seen?
Gingival bleeding, epistaxis, purpura.
72
What internal bleeding manifestations may occur?
Hematemesis, melena, haematuria.
73
What skin findings suggest severe bleeding syndrome?
Extensive ecchymosis.
74
Why is bleeding syndrome particularly dangerous?
Risk of DIC, severe hemorrhage, and multi-organ failure.
75
What are the severe complications of hemotoxic snake envenomation?
Subarachnoid haemorrhage (SAH), intracerebral haemorrhage, and DIC with multiple organ failure.
76
What bedside test is essential in suspected bleeding syndrome?
20-minute whole blood clotting test (20WBCT).
77
What does an abnormal 20WBCT show?
Incoagulable blood, a cardinal sign of consumptive coagulopathy.
78
Which coagulation tests are required in bleeding syndrome?
PT, aPTT, thrombin time, and fibrinogen levels.
79
What does an elevated D-dimer indicate in this context?
Active coagulation and fibrinolysis, supporting DIC.
80
Why is fibrinogen level important in hemotoxic envenomation?
It is consumed, leading to hypofibrinogenemia and bleeding.
81
What additional routine tests should be done?
Urinalysis (hematuria)
U&E/CEU (renal involvement)
FBC (anemia, thrombocytopenia)
82
What antivenom is indicated for boomslang envenomation?
Monovalent boomslang antivenom.
83
Why is monovalent antivenom preferred for boomslang bites?
It is highly specific and effective against boomslang hemotoxic venom.
84
Does antivenom reverse established bleeding?
No — it stops further venom activity, so early administration is critical.
85
What is meant by syndrome overlap in snakebite
Presence of features from more than one syndrome (PPS, PW, Bleeding) in the same patient.
86
Which snakes commonly cause pain/swelling with neurotoxic features?
Non-spitting cobras.
87
What are the early features of this overlap syndrome?
Initial local pain and swelling at the bite site.
88
What neurotoxic symptoms develop 2–3 hours post-bite?
Paraesthesia of tongue and lips
Blurred vision
Loss of smell and taste
Dysphagia
89
What neuromuscular feature may follow?
Progressive muscle weakness.
90
Which snakes have both neurotoxic and cytotoxic venom activity?
Rinkhals
Berg adder
Other small adders
91
What clinical pattern is seen with mixed venom activity?
Local tissue injury plus neurological symptoms.
92
What is the cornerstone of management in syndrome overlap?
Supportive therapy, guided by dominant clinical features.
93
Why is close monitoring essential in overlap syndromes?
Because neurotoxicity may progress rapidly, leading to respiratory failure.
94
What are the two main phases in snakebite treatment?
Pre-hospital management
Emergency Department (ED) management
95
What general principle guides pre-hospital snakebite care?
ABCDE principles.
96
Which traditional first-aid methods are NOT evidence-based in snakebite?
Electrical shock
Suction
Cutting/incision
Cold/ice
Denaturing agents
97
Why is keeping the patient calm important after a snakebite?
Reduces heart rate and venom distribution, especially with Elapid (neurotoxic) bites.
98
What is the role of arterial tourniquets in snakebite?
Limited indications only — generally not recommended.
99
Is pressure bandaging routinely recommended in South Africa?
No — its benefit is speculative in SA settings.
100
How should eye envenomation be managed pre-hospital?
Immediate copious washout with water or bland fluid for ≥30 minutes.
101
What is the cornerstone of ED management of snakebites?
Supportive management.
102
What does supportive management include in snakebite patients?
Airway and ventilation support
Oxygen
IV access and fluids
Monitoring for progression of syndromes
103
What definitive treatment may be required in ED management?
Antivenom, based on clinical syndrome, not snake identification.
104
Why is early ED assessment critical in snakebite patients?
Symptoms may evolve hours after the bite, especially neurotoxicity and bleeding.
105
What proportion of snakebites can be managed without antivenom?
About 90%.
106
Why must the risks and benefits of antivenom be carefully weighed?
Risk of anaphylaxis and serum sickness.
107
Is antivenom a life-saving drug?
Yes — when correctly indicated.
108
When is antivenom indicated in snakebite?
To:
Save life
Stop progression of rapid swelling
Prevent or reverse respiratory failure
Stop bleeding
109
What neurotoxic feature mandates antivenom?
Inability or impending inability to breathe.
110
What cytotoxic feature mandates antivenom?
Rapidly progressive swelling threatening limb or life.
111
What haemotoxic feature mandates antivenom?
Active bleeding or incoagulable blood.
112
What types of antivenom are locally manufactured in South Africa?
Polyvalent antivenom
Monovalent boomslang antivenom
113
When is polyvalent antivenom indicated?
Anticipated severe envenomation
Presence of severe envenomation
114
Why is polyvalent antivenom commonly used?
It covers multiple medically important snakes when the species is unknown.
115
Does antivenom reverse established tissue damage?
No — it halts progression, so early use is critical.
116
What does “anticipated severe envenomation” mean?
Early clinical features suggesting high risk of rapid deterioration, requiring urgent antivenom.
117
What PPS finding suggests severe envenomation within the first hour?
Rapid swelling ≥15 cm within 1 hour.
118
What limb swelling pattern predicts severe PPS?
Swelling reaching the elbow or knee within 3–4 hours
119
What triad suggests anticipated severe neurotoxic envenomation?
Perioral paraesthesia
Excessive salivation
Sweating and/or difficulty breathing
120
Why is this PW triad dangerous?
Indicates early bulbar and respiratory muscle involvement → impending respiratory failure.
121
What local bleeding sign suggests severe hemotoxic envenomation?
Continuous oozing from fang puncture sites.
122
What neurological symptoms suggest severe bleeding syndrome?
Severe headache, dizziness, loss of consciousness, or convulsions.
123
What do these neurological symptoms indicate in bleeding syndrome?
Possible intracranial haemorrhage.
124
What is the management implication of anticipated severe envenomation?
Immediate antivenom + aggressive supportive care.
125
126
What does “severe envenomation present” mean?
Established, life- or limb-threatening toxicity requiring urgent antivenom + intensive supportive care.
127
What limb swelling defines severe PPS?
Swelling of the entire limb within 8 hours.
128
What limb finding indicates compartment syndrome in PPS?
Very tense limb.
129
What vascular complication signals severe PPS?
Compressed major blood vessel (vessel entrapment).
130
What airway-related feature indicates severe PPS?
Airway threatened by swelling.
131
What respiratory symptom in PPS is concerning?
Unexplained shortness of breath after a snakebite.
132
What coagulation finding may coexist with severe PPS?
Abnormal blood clotting post-bite.
133
What respiratory feature defines severe PW without PPS?
Shortness of breath in the absence of PPS (classically non-spitting cobras).
134
What bulbar symptom defines severe PW?
Inability to swallow saliva.
135
What combination suggests severe PW with PPS?
Generalized weakness in the presence of PPS (non-spitting cobras).
136
Which ocular signs alone are unlikely to progress to respiratory failure?
Ptosis, squint, and dilated pupils.
137
What bleeding pattern defines severe hemotoxic envenomation?
Acute systemic bleeding.
138
What bedside test confirms severe bleeding?
20-minute whole blood clotting test showing non-clotting blood in a clean, dry tube.
139
What lab findings indicate severe bleeding syndrome?
Severely abnormal coagulation studies (e.g., markedly deranged PT/aPTT, low fibrinogen).
140
What is the immediate management when severe envenomation is present?
Immediate antivenom, airway/ventilatory support, and ICU-level monitoring.
141
What is the first priority in neurotoxic snake envenomation?
Adequate oxygenation and assisted ventilation.
142
When is airway intervention required in neurotoxic envenomation?
Early intubation and mechanical ventilation if respiratory weakness is present or anticipated.
143
What supportive therapies are used in neurotoxic envenomation?
Sedation and analgesia.
144
How should muscle relaxants be used in neurotoxic envenomation?
With caution, due to risk of worsening respiratory paralysis.
145
When is antivenom indicated in hemotoxic envenomation?
Severe coagulopathy or active bleeding.
146
Are heparin or fibrinolytic agents indicated in venom-induced coagulopathy?
No — they are not indicated.
147
Why is heparin ineffective in venom-induced coagulopathy?
Venom-induced “thrombin” is poorly susceptible to heparin compared to physiological thrombin.
148
Should fibrin-stabilising or thrombolytic drugs be used?
No — they worsen bleeding risk.
149
What proportion of South African snakes are venomous?
Only ~10%.
150
Are traditional first-aid measures effective in snakebite?
No — they are not evidence-based.
151
What single intervention saves the most lives in neurotoxic bites?
Assisted ventilation.
152
What is the recommended approach when the snake is unidentified?
Syndromic approach
153
Do most snakebite patients require antivenom?
No — the majority can be managed without antivenom.
154
How should antivenom be administered?
Intravenously, with the same dose for adults and children.
155
Why do paediatric snakebite cases require special attention?
They require urgent recognition and aggressive management due to rapid deterioration.
General Medicine
flashcards
Decks in class (37)
# Cards
-
EOB Exams659
-
ECG Module 196
-
ECG Module 2153
-
ECG Module 3: normal sinus rhythm284
-
ECG Module 4: Wave abnormalities324
-
ECG Module 5: Rhythm abnormalities243
-
Chest X- ray165
-
Hypertension52
-
Advanced Airway Management341
-
CPR48
-
Post Cardiac Arrest Care35
-
CardioPulmonary Resuscitation532
-
Basic Airway Management122
-
Capnography41
-
Ventilator Settings27
-
Ventilation15
-
Anaphylaxis130
-
Cardiac Infections75
-
Benzodiazepine Overdose112
-
Iron Overdose92
-
Opioid Overdose122
-
Paracetamol Overdose107
-
TCA Overdose80
-
Bradycardia198
-
Tachycardia251
-
Hyponatremia121
-
Hyperthermia27
-
Hypothermia71
-
Hypertensive Emergency146
-
Delirium127
-
Sepsis105
-
Status Epilepticus108
-
Snack bites155
-
Acute Kidney Injury101
-
Pneumonia22
-
Bronchiectasis23
-
COPD40
