EMERGENCIES

•Anaphylaxis
•Endocrine Emergencies
•Haemorrhage

Roshana Mallawaarachchi
19/07/2010
 Anaphylaxis
What is Anaphylaxis?
An acute multi-system severe type I
hypersensitivity reaction.

What is Type 1 Hypersensitivity?

An allergic reaction provoked by reexposure
to a specific type of antigen.
 Anaphylaxis
Type 1 Hypersensitivity
Exposure may be by ingestion, inhalation, injection, or direct
contact.
What is difference between a normal immune response
and a type I hypersensitive response?

Type 1 Hypersensitivity:
Plasma cells secrete IgE.
These antibodies bind to surface of tissue mast cells and
blood basophils.
Mast cells and basophils coated by IgE are "sensitized”.
 Anaphylaxis
Type 1 Hypersensitivity
Later exposure to the same allergen,
Degranulate and the secrete active mediators such as
histamine, leukotriene and prostaglandin.

Effect:
Vasodilation and smooth-muscle contraction.
 Anaphylaxis
Classification of Anaphylaxis
1. Biphasic anaphylaxis
2 . Anaphylactic shock
3. Pseudoanaphylaxis
4. Active anaphylaxis
5. Passive anaphylaxis
 Anaphylaxis
Biphasic Anaphylaxis:
Recurrence of symptoms within 72 hours with no further
exposure to the allergen.
It is managed in the same manner as anaphylaxis.

Anaphylactic Shock:
Anaphylaxis associated with systemic vasodilation which
results in low blood pressure.
Associated with severe bronchoconstriction.
 Anaphylaxis
Pseudoanaphylaxis:
Does not involve an allergic reaction but is due to direct mast
cell degranulation.
This occurs on the first exposure
Eg: Morphine, radiocontrast, aspirin and muscle relaxants.
Treatment is same as anaphylaxis.

Active anaphylaxis:
Active anaphylaxis is what is naturally observed.
After exposed to certain allergens, active anaphylaxis would
be elicited upon exposure to the same allergens.
 Anaphylaxis
Passive anaphylaxis:
Transfer of the serum from sensitized person with certain
allergens.

Passive anaphylaxis would be provoked in the recipient after

exposure to the same allergens.
 Anaphylaxis
Signs and symptoms:
Due to the systemic effects of histamine release.
Usually develop over minutes to hours.

Common areas affected include:

Skin (80% to 90%)
Respiratory (70%)
Gastrointestinal (30% to 45%)
Heart and vasculature (10% to 45%)
Central nervous system (10% to 15%)
Skin
Anaphylaxis
Generalized hives, itchiness, flushing, and swelling of the lips,
tongue or throat.

Respiratory
Shortness of breath, wheezes or stridor, and low oxygen.

Gastrointestinal
Crampy abdominal pain, diarrhea, and vomiting.
Cardiovascular
Anaphylaxis
Histamine - coronary artery spasm - myocardial infarction or
dysrhythmia.

Nervous system
Low blood pressure - lightheadedness and loss of
consciousness.
Loss of bladder control and muscle tone.
Anxiety.
 Anaphylaxis
What are the causes?
•Foods – Peanut, Fish, Egg, Milk

•Drugs – Any medication may trigger anaphylaxis.

Antibiotics (β-lactam antibiotics)
Aspirin, ibuprofen, and other analgesics.
Morphine, Some vaccinations, x-ray contrast (Pseudoanapylaxis)

•Venom – Insect stings (Bee, Wasp)

 Anaphylaxis
Diagnosis:
Based upon symptoms that occur suddenly after being exposed
to a potential trigger.

Apart from its clinical features, blood tests for tryptase (released
from mast cells) may be useful.

Patch test may help to identify the cause.

 Anaphylaxis
Mangement:
Secure the airway. –Give 100% Oxygen
Intubate if respiratory obstruction.

Remove the cause.

Raise the feet may restore the circulation.

Give adrenaline IM 0.5mg (0.5ml 1:1000 solution)

Repeat every 5 min. (If no clinical improvement)
 Anaphylaxis
Mangement: (Cont…)
Secure IV access.

Chlorphenaramine 10mg IV
Hydrocortizone 200mg IV

IV Fluids (0.9% saline) – up to 2L may be needed.

Titrate against Blood pressure.

If wheeze – Treat for asthma (Beta 2 agonist)

If still hypotensive, admission to ICU.
 Anaphylaxis
Further Management:
Admit to ward. Monitor ECG.
Continue chlorphenaramine. 4mg/6h

Can encourage to carry prefilled adrenaline syringe for self

administration.
 Adrenaline
•Adrenaline is a Hormone, catecholamine, produced by the
adrenal gland.
•It increases heart rate, contracts blood vessels and dilates
airway.
•Causes smooth muscle relaxation in the airways, but causes
contraction of the smooth muscle in arterioles.
Organ Effect
Heart Increase Heart rate
Lungs Increase respiratory rate
All Tissues Vasoconstriction or Vasodilation
Liver Stimulate glycogenolysis
Sytemic Triggers lipolysis, Muscle contraction
Therapeutic use:
Adrenaline
1. Cardiac arrest - Increase peripheral resistance via α1
receptor-dependent vasoconstriction and to increase cardiac
output.
2. Shock and anaphylaxis - Vasoconstrictive effect.
3. Use in local anesthetics - as a vasoconstrictor to reduce the
absorption - prolong the action of the anesthetic agent.
Eg:Lidocaine

Side Effects:
Palpitations, tachycardia, arrhythmia, anxiety, headache,
tremor, hypertension, and acute pulmonary edema.
 Endocrine Emegencies
1. Diabetic Ketoacidosis
2. Hyperglycaemic Hyperosmolar non-ketotic coma
3. Addisonian Crisis
 Diabetic Ketoacidosis
Life threatening complication in patients with Diabetes mellitus.
Predominantly in those with type 1 diabetes.
Uncontrolled catabolism due to insulin deficiency.

• Absence of insulin;
• Hepatic Glucose production increase.
• Peripheral uptake is reduced.
• Rising Glucose levels leads to an osmotic diuresis.
• Loss of fluids and electrolytes, and dehydration.
• Rapid lipolysis, leading to elevated FFA.
• This Free Fatty acids (FFA) is converted to ketone bodies.
• Accumulation of ketone bodies produces metabolic acidosis.
 Diabetic Ketoacidosis
Vomiting leads to further loss of fluids.
Excess ketones excreted in urine and respiratory system.
Respiratory compensation for the acidosis leads to
Hyperventilation.

Clinical Features:
Hyperventilation (Kussmaul respiration)
Ketotic breathe
Nausea and Vomiting
Abdominal pain
Confusion, Coma
Dehydration
 Diabetic Ketoacidosis
Diagnosis:
Confirmed by demonstrating Hyperglycaemia with ketonaemia
or heavy ketoneuria and acidosis.

Treatment should be started as soon as the first blood sample

has been taken.

Investigation:
• Blood glucose
• Urea and Electrolytes
• ABG
• Urine: Ketones
• ECG
 Diabetic Ketoacidosis
Management:
IV access and start Fluids. (0.9% Saline)
Check plasma glucose: Usually >20mmol/l
If so give 4-8units Soluble insulin IV

NG tube nauseated/Vomiting
Potassium replacement – 20mmol KCL per litre.
Adjust [KCL] depending on electrolytes.

pH below 7, give Sodium bicarbonate.

 Diabetic Ketoacidosis
Management:
When blood glucose falls to 10-12 mmol/l swap fluids to 5%
dextrose.

Once stable and able to drink transfer patient to 4X daily

subcutaneous insulin.

If infection – Broad spectrum Antibiotics

Catheterization
Prophylactic Heparin in comatose.
Hyperglycaemic Hyperosmolar
non-ketotic coma
Only those with Type 2 DM.
History is longer. (1 week)
Marked dehydration and Glucose >35mmol/l
Acidosis is absent, as there is no switch to Ketone metabolism.
Osmolality is >340mosmol/kg

Focal CNS signs may occur.

The risk of DVT is high. So give IV Heparin.
Hyperglycaemic Hyperosmolar
non-ketotic coma
Precipitating factors:
Glucose rich fluids
Medication such as Thiazide and steroids.
Management:
Rehydrate over 48hrs. With 0.9% saline.
Avoid half normal saline (0.45%) since rapid dilution of the
blood may cause more cerebral damage.
Insulin may not be needed.
 Addisonian crisis
Severe adrenal insufficiency.

Causes:
Addison's disease
Adrenal hemorrhage
Infection
Trauma
Long term oral Glucocorticoids, who stop treatment suddenly.

Untreated addisonian crisis can be fatal.

Medical emergency.
 Addisonian crisis
Symptoms:
Sudden penetrating pain in the legs, lower back or abdomen
Severe vomiting and diarrhea, resulting in dehydration
Low blood pressure
Syncope (loss of consciousness)
Hypoglycemia
Confusion, psychosis, slurred speech
Severe lethargy
Hypercalcaemia
Convulsions
Fever
 Addisonian crisis
Management:
If suspected, treat before biochemical results.
Take blood for cortisol and ACTH.

IV Hydrocortisone 100mg stat.

IV Fluids

Monitor blood glucose and Glucose should be infused if

Hypoglycaemic.

Give Antibiotics.
 Haemorrhage
Types of Haemorrhage:
• Arterial – Bright red, Emitted as a spurting jet.
• Venous – Dark red, steady and copious flow.
• Capillary – Bright red, rapid.
• Primary Haemorrhage – Occurs at the time of injury or operation.
• Reactionary Haemorrhage – Follow primary Haemorrhage within
24 hours. It is mainly due to slipping of ligature, dislodgement of
clots.
• Secondary Haemorrhage - Occurs after 7-14 days and is due to
infection. Eg: Presence of a fragment of tooth.
• External Haemorrhage
• Internal Haemorrhage - Ruptured spleen, Liver. Fractures.
 Haemorrhage
Four classes by the American College of Surgeons.
1. Class I - up to 15% of blood loss. There is typically no
change in vital signs and fluid resuscitation is not usually
necessary.
2. Class II –
• 15-30% of total blood loss.
• Often tachycardic.
• Narrow Pulse pressures.
• Compensate with peripheral vasoconstriction.
• Skin may look pale and be cold.
• Volume resuscitation with crystalloids
• (Saline solution or Lactated Ringer's solution)
• Blood transfusion is not typically required.
 Haemorrhage
3. Class III –
• Loss of 30-40% blood volume.
• Low blood pressure
• Increase heart rate
• Peripheral hypoperfusion (shock)
• Delayed capillary refill
• Mental status worsens
• Fluid resuscitation with crystalloid and blood
transfusion are usually necessary
 Haemorrhage
4. Class IV –
• Loss of >40% of circulating blood volume.
• The limit of the body's compensation is reached.
• Aggressive resuscitation is required to prevent death.
 Haemorrhage
Methods of determining blood loss:
Blood clot – A clot the size of clenched fist is roughly 500ml.
Swelling of the closed fracture
Swab weighing – By weighing the swabs after use and substracting
the dry weight. (1g = 1ml)
Haemoglobin level – Normal value 10-12 g/dl. There is no immediate
change, but after some hours, the level falls as a result of influx of
interstitial fluid.
Measurement of central venous pressure.
 Haemorrhage
Causes:
Traumatic injuries – Abrasions, Incision, Laceration, Head
injuries, Dental extraction
Medical conditions –
• Vitamin K deficiency
• Von Willebrand disease
• Haemophilia
• Thrombocytopenia
• End-stage Liver failure
Drugs – NSAIDs, Warfarin
 Haemorrhage
It is possible to bleed to death following the extraction of a
tooth.

Excessive bleeding can occur in patients with,

Anticoagulant drugs
Bleeding disorders like Hemophilia
 Haemorrhage
Treatment:
Should be treated urgently.
Minimize further blood loss by pressure and packing, position
and rest. Operative procedure (Ligation)
Fluid resuscitation – Blood transfusion, Infusion of Albumin,
Gelafundin, Dextran.
Thank You…!