Medical emergencies OMFS.ppt

of 72/72
PREVENTION PREVENTION When you prepare for an emergency, the When you prepare for an emergency, the emergency cease to exit” emergency cease to exit” Detail medical history Detail medical history Physical and Psychological evaluation Physical and Psychological evaluation Determination of medical risk Determination of medical risk Physical status classification system (1962, American Physical status classification system (1962, American Society of Anesthesiologists) Society of Anesthesiologists) ASA I – A patient without systemic disease, a ASA I – A patient without systemic disease, a normal healthy patient normal healthy patient ASA II – A patient with mild systemic disease ASA II – A patient with mild systemic disease ASA III – A patient with severe systemic disease ASA III – A patient with severe systemic disease that limits activity but is not incapacitating that limits activity but is not incapacitating ASA IV – A patient with incapacitating systemic ASA IV – A patient with incapacitating systemic disease that is a constant threat to life. disease that is a constant threat to life. ASA V – A moribund patient not expected to survive ASA V – A moribund patient not expected to survive 24 hrs with or with out surgery. 24 hrs with or with out surgery. ASA VI – Clinically dead patient being maintained ASA VI – Clinically dead patient being maintained
  • date post

  • Category


  • view

  • download


Embed Size (px)

Transcript of Medical emergencies OMFS.ppt


When you prepare for an emergency, the emergency cease to exit Detail medical history

Physical and Psychological evaluation Determination of medical risk Physical status classification system (1962, American Society of Anesthesiologists) ASA I A patient without systemic disease, a normal healthy patient

ASA II A patient with mild systemic disease ASA III A patient with severe systemic disease that limits activity but is not incapacitating ASA IV A patient with incapacitating systemic disease that is a constant threat to life. ASA V A moribund patient not expected to survive 24 hrs with or with out surgery. ASA VI Clinically dead patient being maintained for harvesting organs.

CLASIFICASSION OF EMERGENCIES1. NON-CARDIOVASCULAR EMERGENCIES A. Stress related Vasodepressor syncope Hyperventilation syndrome. Acute adrenal insufficiency Asthma Hypoglycemic reactions. Epilepsy Thyroid crisis B. Non Stress related Orthostatic hypotension Overdose reaction. Hyperglycemia Allergy. 2. CARDIOVASCULAR EMERGENCIES A. Stress related Angina pectoris Acute Myocardial Infraction Heart failure Cerebral ischemia and infraction B. Non Stress related Acute myocardial infraction

VASODEPRESSOR SYNCOPESyncope is a general term referring to a sudden, transient loss of consciousness, usually secondary to cerebral ischemia. Factors that Can precipitate vasodepressor syncope may be divided into two groups. 1. Psychogenic Fright 2. Non psychogenic Upright or standing position Hunger Exhaustion Hot, humid environment

Anxiety Emotional stress Pain Sight of blood Sight of surgical instruments

Clinical manifestation of syncope can be divided in to two phases

1. Presyncope Feeling of warmth in face and neck Loss of color : Pale Heavy perspiration Nausea

2. Syncope Pupillary dilation Hyperpnea

Hypotension Bradycardia Visual disturbances Dizziness Convulsive movement and muscular twitching Loss of consiousness

Rapid heart rate Pupillary dilation BP and heart rate become depressed

PATHOPHYSIOLOGYVasodepressor syncope is most commonly caused by a decrease in cerebral blood flow below a critical level and is usually characterized by a sudden fall in blood pressure and slowing of the heart rate

PATHO PHYSIOLOGY AND MANIFESTATION:ANXIETY Incresed catecholomine release Decreased peripheral vascular Resistance. Pooling of blood in periphery decreased arterial blood pressure. Compensatory mechanisms cause increased heartrate, feeling of warmth , pallor, perspiration, rapid breathing due to fatigue of compensatory mechanism. Reflex vagally Decompensation Mediated bradycardia, nausea, Occurs weakness & hypo tension Reduced cerebral blood flow Light headeness syncope if prolonged seizure activity

MANAGE MENTPRODROME: 1. Terminate all dental treatment. 2. Position patient in supine posture ,with legs raised above the level of head 3. Attempt to calm the patient 4. Cool towel to forehead. 5. Monitor vital signs

Syncopal episode: 1. Terminate all dental treatment. 2. Patient in supine position with legs raised.

3. Check for breathing.

If absent , Consider other causes of syncope including hypo glycaemia cerebrovascular accident , cardiac Dysarrhythmia etc

If present , - Start BLS crush ammonia under the nose - Summon medical assistance administer oxygen -Monitor vital signs - plan anxiety control measure.

ORTHOSTATIC HYPOTENSIONOrthostatic hypotension may be defined as disorder of autonomic nervous system in which syncope occurs when patient assumes upright position. Predisposing factors

Drug administration and ingestion Inadequate postural reflex Pregnancy Venous defect in legs Addison's disease Chronic orthostatic hypotension ( Shy Drager syndrome)


Type of hypotension Orthostatic

Manifestation - Mild to no signs and symptoms of vasodepressor syncope - Low blood presure - Higher heart rate - Loss of consciousness without any sign and symptoms

Chronic orthostatic

PATHOPHYSIOLOGYOccurs :- because of peripheral pooling of blood which is not remobilised quickly enough to prevent cerebral ischaemia when a patient rapidly assumes an upright posture. Patient feels light headed /syncopal The usual reaction of cardiovascular system when a person is tilted from the supine to the erect position is an immediate drop in the systolic blood pressure of from 5 to 40 torr, but an equally rapid rise occurs so that within 30 seconds the pressure become normal or slightly higher than supine position.

In orthostatic hypotension bodys compensatory mechanism fail to compensate for pressure change. And resulting hypotension may cause cerebral ischemia which leads to loss of consciousness.

MANAGEMENT:1. Terminate all dental treatment. 2. Patient in supine position with legs raised above the level of head 3. Monitor vital sign 4. Once blood pressure returns , slowly shift the patient to sitting .posture 5. Discharge to home once vital signs are normal & stable 6. Obtain medical consultalion before any further dental care.

Patients with predisposition to orthostatic hypotension are, the ones receiving medications.

Drugs which produce intra vascular depletion such as dieuretics. Drugs that produce peripheral vasodilatation such as non dieuretic anti hypertensives, narcotics, psychiatric drugs. Drugs which prevent the heart rate from increasing reflexly. such beta sympathetic blockers. Eg:- propalanol.

These patients should be managed by allowing a much longer period to attain standing position ie,by stopping at several increments before attaining upright posture, to allow cardio vascular compensation to occur. If the patient was sedated by using long acting narcotics , an antagonist such as nalaxone may be necessary .

ASTHMAIt is a clinical state of hypersensitivity of trachobronchial tree characterized by recurrent paroxyms of dyspnea and wheezing, which are the result of bronchospasm, bronchial wall edema and hypersecretion of mucous glands. It has three characteristics : 1. Airflow limitation which is usually reversible spontenouly or with treatment. In chronic asthma inflammation may lead to irreversible airflow limitation. 2. Airway hyper responsiveness to wide range of stimuli

3. Inflammation of bronchi with eosinophils, T-lymphocytes and mast cells with associated edema, smooth muscle hyper trophy and mucous plugging

Asthma can be classified according to etiological factors :

1. Extrinsic2. Intrinsic

PATHOPHYSIOLOGYIn the asthmatic patient there is a continuous state of hyperreactivity of the bronchi, during which exposure to any of a wide variety of bronchial irritants may precipitate an acute attack. Asthmatic attack may be provoked 1. Immune reactions (Allergic)

2. By substance directly toxic or irritating to bronchial mucosa.3. Through combination of these two mechanism


MANIFESTATIONin chest Spell of couch Wheezing Dyspnea Rise in blood pressure Rise in heart rateIntense

Severe episode

dyspnea and orthopnea Cynosis of mucous membranes Perspiration Flushing of face Use of accessory muscle of respiration Fatigue Mental confusion

Status asthamaticusStatus asthmatic is a state in which the acute asthmatic episode persists in spite of drug therapy. Pt. with status asthmaticus most commonly exhibit signs of extreme fatigue, dehydration, severe hpoxia, cynosis, peripheral vascular shock

INVESTIGATION 1. Lung function tests

2. PEFR3. Histamine inhalation 4. Peripheral blood 5. Skin tests


MANAGEMENT:1. Terminate all dental treatment. 2. Monitor vital sign 3. Bronchodilator by spray Meteprotereral Isoproterenal Epinephrine 4.Administer O2

Sitting position

Signs and symptoms relieved Monitor during recovery DiscontinueanyIVline provide no dental tretment until patients physian approves.

Continues. Give epinephrine 0.3ml of 1:10000IM/SC start IV & drip of crystalloid solution. Monitor vital signs. Signs and symptoms not relieved call medical assistance Start theophylline IV, 250mg given over 10 mins Cortisone 100mg IV Prepare for transport to emergency care facility.


Hyper ventilation is defined as ventilation inexcess of that require to maintain normal blood PaCo2 & PaO2. It may be produced by an incerase in either the frequency of depth of respiration or by a combination of two.

Causes1. Anxiety 5. Hypercapnia

2. Pain3. Metabolic acidosis 4. Drug intoxication

6. Cirrhosis7. Organic CNS disease

CLINICAL MANIFESTATION1. Cardiovascular Palpitations Tachycardia Precordial discomfort 2. Neurological Dizziness Lightheadedness Numbness and tingling of extremities Tetany (rare) Convulsion 3. Respiratory Shortness of breath Chest pain 4. Musculoskeletal Muscle pain and cramp

Tremors Stiffness Tetany

PATHOPHYSIOLOGYSigns and symptoms of hyperventilation may be due to :

1. Respiratory alkslosis

2. Increased blood level of cathecolamines3. Decreased in level of circulating ionized calcium

MANAGEMENT : 1. Terminate all dental procedures and remove any foreign body from the mouth 2. Patient in upright position 3. Attempt to verbally calm the patient 4. Have the patient breathe CO2 enriched air such as in and out of paper bag. 5. If symptoms persist , administer diazepam 10mg IM/IV untill anxiety relieved. 6. Monitor vital signs 7. perform all further dental surgery using anxiety reducing measures.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE. - Many of these patients depend on maintaining an upright posture to breathe adequately. - They become accustomed to having high arterial CO2 levels & low level of blood O2 as primary stimulus to drive respirations. - Many of these patients experience difficulty if placed in supine position/or if placed on high flow nasal oxygen.

TREATMENT: Discontinue O2 administration If apnoea persists, artificial ventilation and emergency assistance is given.

FOREIGN BODY ASPIRATION: Aspiration of foreign bodies into the air ways is always a potential problem during oral surgical procedures.

-This is especially true if the patient is positioned supine /semierrect in the chair or is sufficiently sedated to dull the gag reflex. .Objects that fall into hypopharynx ,pass harmlessly through gastro intestinal tract. .Even if the clinician feels confident that the material was swallowed ,a chest radiograph must be taken.

Occasionally the foreign object is aspirated into larynx, where in lightly sedated/ non sedated patient violent coughing will ensue. - Patients can still talk & breathe. If larger objects are aspirated, it obstructs the airway & becomes lodged in such away that coughing is ineffective

MANAGEMENT:1. Terminate all dental treatment. 2. Patient in sitting position 3. Assist patient to try to cough object out

Patient becomes unconscious

Patient remains conscious.

1. Summon medical assistance 2. Place patient in supine position 3. Begin abdominal thurst followed by turning patient on side & using finger to sweep oral cavity for foreign object . 4. Attempt to ventilate

symptoms persist -Heimlich maneuver. -Administer O2 - summon medical assistance. - Monitor vital signs - Transport to emergency care.

NO symptoms Observe for one hour.

Able ventilate Start BLS Administer O2 Transport to Emergency.

Unable to ventilate Repeat step 3&4 Laryngoscopy Cricothyrotomy.


Anaphylaxis is the classical type-I immediate hypersensitivity reaction. Anaphylaxis is an amplified, harmful immunologic reaction that occurs after reexposure to an antigen. It is the opposite of prophylaxis, or immunologic protection that results from prior antigen exposure. True anaphylaxis is a systemic reaction caused by antigen-specific cross-linking of IgE molecules on the surface of tissue mast cells and peripheral blood basophils, which results in the immediate release of potent mediators.


1. 2.

Skin: Intense itching Flushing Conjunctivitis Pruritus Urticaria Erythema Gastrointestinal and genitourinary Abdominal cramp Nausea & vomiting Fecal and urinary incontinence




Feeling of tightness in the chest Cough Wheezing Dyspnea Cynosis Laryngeal edema Cardiovascular Pallor Palpitation Tachycardia Hypotension Cardiac Dysrhythmia Loss of consciousness Cardiac arrest


Pathophysiology of anaphylaxis is divided in to two phase 1. Sensitizing phase.2. Challenging phase.

1. Sensitizing phase.

During the sensitizing phase the patient receive the initial exposure to the antigen. In response to antigen plasma cells produce immunoglobulins (IgE) specific for that particular antigen. This IgE antibodies attach them selves to the cell membrane of circulating basophils and tissue mast cells.2. Challenging phase

Subsequent exposure to the antigen results in an antigenantibody interaction thought to be initiated by the bridging of two adjacent IgE molecules on the surface of the mast cells and basophils, resulting in release of some pharmacologically active substances which are responsible for the clinical picture of the anaphylaxis.


Primary mediators Histamine

Serotonin Eosinophil chemotatic factor of anaphylaxis Slow reacting substance of anaphylaxis

Secondary mediators of anaphylaxis

These includes two groups of compounds Lipid mediators Cytokines

Lipid mediators

Leucotrines C4 & D5 Prostagladin D2

Platelet activating factor. Cytokines

Mast cells produced cytokines(TNF,IL-1,IL-4,IL-5)


1. Skin test: The characteristic skin response in Wheal & Flare The skin response takes 5-15 mins to develop and may persist for 30 mins. In skin test 0.02-0.03 ml of allergen injected SC. Normally 4*4 mm wheal in adult and 3*3 mm wheal in children can be considered a positive response to skin test.

Skin test is evaluated by the size of the wheal

2. Patch test: -

This test include application of a patch of 10mml on 2.5cm2 gauze that stays on the skin for 2 days.After 2 days biopsy is taken from that area.

A positive patch response induces macroscopic eczema and an infiltrate of cells into the dermis. Cellular infiltrate include eosinophils,basophiles and lymphocytes

First-line therapy

Airway maintenance Epinephrine: - SC: 0.01 mL/kg, to maximum of 0.3 to 0.5 mL, of 1:1,000 aqueous solution (1 mg/mL) Fluids: -5% human albumin solution, or 5% dextrose in 0.5N saline solution or lactated Ringer's injection.

Second-line therapy

Antihistamines : -Antihistamines are useful as second-line

therapy when a prolonged course is suspected. Diphenhydramine hydrochloride can be given orally, intramuscularly, or intravenously at a dose of 1 mg/kg up to a maximum of 50 mg every 6 hours. Corticosteroids : -Hydrocortisone 100mg I.V. Bronchodilators : -Salbuterol,IV aminophylline 5 6mg/kg over 20 mins

ACUTE ADRENAL INSUFFICIENCY The adrenal cortex produces and secretes over 30 steroid hormons most of which lake any identifiable biologic activity. Cortisol is one of the most important product of adrenal cortex it is consider as life saving hormone as its wide spread effect Hyposecretion of cortisol may produce life threatening situation. There are two types of adrenal insufficiency 1. Primary adrenal insufficiency 2. Secondary adrenal insufficiency.


Major predisposing factor in all type of adrenal insufficiency is lack of glucocorticsteroid hormone which develop through several mechanisms.1. Following sudden withdrawal of steroid hormones in pt. who has primary adrenal insufficiency 2. Following sudden withdrawal in a pt. with normal adrenal cortices but with a temporary insufficiency resulting from cortical supression by exogenous corticosteroid administration

3. Following stress such as physiologic & psycologic4. Following bilateral adrenalectomy or removal of functioning adrenal tumour 5. Sudden destruction of pituitary gland. 6. Following injury to the both adrenal gland by trauma, harmorrhage, infection, thrombosis or surgery.


1. Mental confusion 2. Muscle weakness 3. Intense pain in abdomen 4. Hypoglycemia 5. Extreme fatigue 6. Nausea & vomiting

7. Hypotension 8. Syncopal episode 9. Coma 10.Hyperpigmentation

11.Loss of weight12.Craving for salt and water


pathogenesis Four Stages in Adrenal Insufficiency 1.High plasma renin, low aldosterone 2. Impaired cortisol response to ACTH stimulation 3. Increased morning ACTH w/ normal cortisol 4.Low morning serum cortisol Therefore, almost complete adrenal destruction has occurred by the time low cortisol levels develop


1. Treminate all the treatment.2. Position the pt. (Supine) 3. Administer O2 4. 100 mg Hydrocortisone IV over 30 seconds 5. Establish IV line, IV infusion of 5% dextrose + 100mg of hydrocortisone over the period of 2 hrs 6. For severe hypotension administer 0.3 to 0.5 mg epinephrine IM or IV

The Rule of Twos states that adrenal suppression may occur if a patient is taking 20 mg of cortisone or its equivalent daily, for 2 weeks within 2 years of dental treatment . In order to avoid an adrenal crisis, corticosteroid supplementation was advised

- Patients at risk are generally those who take atleast 20 mg of corticosteroid daily for atleast 2 weeks any time during the year preceeding planned surgical procedure. If adrenal suppression is suspected. 60 mg of hydrocortisone presugically , 40mg the first 2 days after surgery , 20 mg the next 3 days after surgery


Diabetes mellitus is a group of metabolic disorders characterized by chronic hypoglycemia due to relative insulin deficiency.

Predisposing factors

1. Genetic predisposition2. Primary destruction of islets of langerhans in the pancreas causeed by inflammation, cancer or surgery

3. Endocrine condition such as hyperpituitarism or hyperthyrodism4. Administration of steroids.

A metabolic disease in which the patients long term prognosis seems dependent - An untreated insulin dependant diabetic constantly runs the risk of developing -However a common situation the diabetic patients encounter in a dental setting is

upon keeping serum glucose levels close to normal.


hypoglycemia resulting from a mismatch of insulin dose and serum glucose.

Serum glucose concentration in diabetic patients represents a balance between

administered insulin, glucose placed into serum from various sources and glucose utilization.

2 Primary sources of glucose are dietary and gluconeogenisis from adipose

tissue, muscle and glycogen stores.

Serum glucose level can fall because of any or all of following. Increased administered insulin Decreasing dietary caloric intake Increasing metabolic utilization of glucose (exercise , emotional stress) Problems with hypoglycaemia during dental care normally arise because , 1) Patient has acutely decreased his caloric intake. 2) has any infection and /or 3) increased metabolic rate caused by anxiety. If the patient has not compensated for this diminution of available glucose by decreasing the usual dose of insulin, hypoglycemia results

MANIFESTATION OF ACUTE HYPOGLYCEMIA :Mild Hunger Nausea Mood changes Weakness Moderate Severe Tachycardia Hypotension Perspiration unconsciousness Pallor seizures Behavioral Change (Uncooperativeness confusion)

MANAGEMENT :Terminate all dental treament.

Mild - Administer glucose source sugar/fruit juice - Monitor vital signs

Moderate - Monitor vital signs -Administer glucose source. (fruit juice) - If symptoms do not rapidly improve, administer 50ml of 50% Glucose or 1mg glucogon IV or IM.

Severe hypoglycemia

- Administer 50ml of 50% glucose IV/IM or 1mg glucogon. - Summon medical assistance - Monitor vital signs - Administer O2 - Transport to emergency care facility If 50% glucose and glucogon are not available, 0.5ml dose of 1: 1000 epinephrine can be administered subcutaneously and repeated every 15 min as needed

CHEST DISCOMFORT: The appearance of chest discomfort in a patient who may have ischaemic heart disease in peri operative calls for rapid identification of etiology so that appropriate measures can be taken.

Clinical Manifestations of chest pain caused by myocardial ischaemia or infarctions:Discomfort described by patient as being , 1. Squeezing, bursting , pressing, burning , choking &/ or crushing in nature (not sharp/stabbing) 2. Substernally located radiation to left shoulder, arm and /or left side of neck& mandible. 3. Associated with exertion, heavy meal , anxiety. 4. Relieved by vasodilators such as nitroglycerine or rest ( in angina) 5. Accompanied by dyspnoea, nausea,weakness,palpitations,perspiration

Differential diagnosis of acute onset chest pain : Common Causes : Cardio vascular system---- Angina , Myocardial infarction. Gastro intestinal system--- dyspepsia, hiatal hernia, reflux esophagitis gastric ulcers Musculo skeletal system-intercoastal muscle spasm Psychological--------------- hyperventilation

MANAGEMENT:1.Terminate all dental procedures. 2.Position patient in semi reclined posture. 3.Give Trinitroglycerine(TNG) 0.4mg tablet/spray till blood pressure reaches 90mm Hg 4.Administer oxygen. 5.Check pulse +Blood pressure.

Discomfort relieved Assume angina pectoris was present taper O2 over 5 min

continues 3 minutes after TNG Second TNG dose Monitor vital signs Continues 3 min after second TNG dose Give third TNG dose Monitor vital signs Continues 3 min after 3rd Dose of TNG

Assume myocardial infarction.

In that case, 1. Summon medical assistance 2. Start Iv line with drip of crystalloid solution. 3. If severe discomfort is present morphine sulfate 2 mg sc/Iv every 3 min 4. Prepare for transport to emergency care facility

LOCAL ANESTHETIC TOXICITY:Local anesthetics as with all medications, toxicity reactions occur if it is given in an amount or in a manner that produces an excessive serum concentration

Prevention:- Least effective dose to be given - Patients age, lean body mass, liver function, and history of problems with local anesthetics must be considered . - Manner of administration -slow & intra vascular injection should be avoided. - Use of Vasoconstrictors to slow the entry of local anesthetic into the blood. Should be remembered that, topical use of LA in wounds/on mucosal surfaces allows rapid entry of local anesthetics into the systemic circulation. Choice of local anesthetics Local anesthetics vary in their lipid solubility vasodilatory properties , protein binding and inherent toxicity. So the dentist should be knowledgeable about various local anaesthetics.

MANIFESTATIONS AND MANAGEMENT:Mild Toxicity Management Talkativeness, anxiety slurred speech,, confusion Stop administration of LA Monitor vital signs Observe in office for 1 hour.

Moderate Toxicity Stuffering speech, nystagmus, Tremors, headache, dizziness, Blurred vision Drowsiness

Stop giving LA Supine position monitor vital signs , Administer O2 observe in office for 1hr.

Severe Toxicity Seizure ,cardiac dysrrhythmia or arrest

Supineposition. If seizures ,protect from near by object Suction oral cavity in case of vomiting . Summon medical assistance Monitor vital signs. Administer oxygen

- Administer diazepam 5-10mg slowly or midazolam 2-6-mg slowly - Institute BLS if necessary - Transport to emergency care facility