PREVENTIONPREVENTION““When you prepare for an emergency, the emergency cease to exit”When you prepare for an emergency, the emergency cease to exit”

• Detail medical historyDetail medical history

• Physical and Psychological evaluationPhysical and Psychological evaluation

• Determination of medical riskDetermination of medical risk

Physical status classification system (1962, American Society of Physical status classification system (1962, American Society of Anesthesiologists)Anesthesiologists)

ASA I – A patient without systemic disease, a normal healthy patientASA I – A patient without systemic disease, a normal healthy patient

ASA II – A patient with mild systemic diseaseASA II – A patient with mild systemic disease

ASA III – A patient with severe systemic disease that limits activity but is not ASA III – A patient with severe systemic disease that limits activity but is not incapacitatingincapacitating

ASA IV – A patient with incapacitating systemic disease that is a constant ASA IV – A patient with incapacitating systemic disease that is a constant threat to life.threat to life.

ASA V – A moribund patient not expected to survive 24 hrs with or with out ASA V – A moribund patient not expected to survive 24 hrs with or with out surgery.surgery.

ASA VI – Clinically dead patient being maintained for harvesting organsASA VI – Clinically dead patient being maintained for harvesting organs..

CLASIFICASSION OF EMERGENCIESCLASIFICASSION OF EMERGENCIES

1.1. NON-CARDIOVASCULAR NON-CARDIOVASCULAR EMERGENCIESEMERGENCIESA.A. Stress relatedStress related

Vasodepressor syncopeVasodepressor syncope Hyperventilation syndrome.Hyperventilation syndrome. Acute adrenal insufficiencyAcute adrenal insufficiency AsthmaAsthma Hypoglycemic reactions.Hypoglycemic reactions. EpilepsyEpilepsy Thyroid crisisThyroid crisis

A.A. Non – Stress relatedNon – Stress related Orthostatic hypotensionOrthostatic hypotension Overdose reaction.Overdose reaction. HyperglycemiaHyperglycemia Allergy.Allergy.

2.2. CARDIOVASCULAR CARDIOVASCULAR EMERGENCIESEMERGENCIESA.A. Stress relatedStress related

Angina pectorisAngina pectoris Acute Myocardial InfractionAcute Myocardial Infraction Heart failureHeart failure Cerebral ischemia and infractionCerebral ischemia and infraction

B.B. Non – Stress relatedNon – Stress related Acute myocardial infractionAcute myocardial infraction

VASODEPRESSOR SYNCOPEVASODEPRESSOR SYNCOPE

Syncope is a general term referring to a sudden, transient loss of consciousness, Syncope is a general term referring to a sudden, transient loss of consciousness, usually secondary to cerebral ischemia.usually secondary to cerebral ischemia.

Factors that Can precipitate vasodepressor syncope may be divided into two Factors that Can precipitate vasodepressor syncope may be divided into two groups.groups.

1.1. PsychogenicPsychogenic

• FrightFright

• AnxietyAnxiety

• Emotional stressEmotional stress

• PainPain

• Sight of bloodSight of blood

• Sight of surgical instrumentsSight of surgical instruments

2.2. Non psychogenic Non psychogenic

• Upright or standing positionUpright or standing position

• HungerHunger

• ExhaustionExhaustion

• Hot, humid environmentHot, humid environment

• Clinical manifestation of syncope can be divided in to two phasesClinical manifestation of syncope can be divided in to two phases

1.1. PresyncopePresyncope

• Feeling of warmth in face and Feeling of warmth in face and neckneck

• Loss of color : PaleLoss of color : Pale

• Heavy perspirationHeavy perspiration

• NauseaNausea

• Rapid heart rateRapid heart rate

• Pupillary dilationPupillary dilation

• BP and heart rate become BP and heart rate become depresseddepressed

2.2. SyncopeSyncope

• Pupillary dilationPupillary dilation

• HyperpneaHyperpnea

• HypotensionHypotension

• BradycardiaBradycardia

• Visual disturbancesVisual disturbances

• DizzinessDizziness

• Convulsive movement and Convulsive movement and muscular twitchingmuscular twitching

• Loss of consiousnessLoss of consiousness

PATHOPHYSIOLOGYPATHOPHYSIOLOGYVasodepressor syncope is most commonly caused by a decrease in Vasodepressor syncope is most commonly caused by a decrease in cerebral blood flow below a critical level and is usually characterized cerebral blood flow below a critical level and is usually characterized by a sudden fall in blood pressure and slowing of the heart rateby 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 MENTMANAGE MENT

PRODROME: 1. Terminate all dental treatment.2. Position patient in supine posture ,with legs

raised above the level of head3. 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 If present , syncope including hypo glycaemia - Start BLS cerebrovascular accident crush ammonia under the nose , cardiac Dysarrhythmia etc - Summon medical assistance

administer oxygen -Monitor vital signs - plan anxiety control measure.

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

• Predisposing factorsPredisposing factors

Drug administration and ingestionDrug administration and ingestion

Inadequate postural reflexInadequate postural reflex

PregnancyPregnancy

Venous defect in legsVenous defect in legs

Addison's diseaseAddison's disease

Chronic orthostatic hypotension ( Shy – Drager syndrome)Chronic orthostatic hypotension ( Shy – Drager syndrome)

CLINICAL MENIFESTATION OF ORTHOSTATIC HYPOTENSION

Type of Type of hypotensionhypotension ManifestationManifestation

OrthostaticOrthostatic - Mild to no signs and - Mild to no signs and symptoms of vasodepressor symptoms of vasodepressor syncopesyncope- Low blood presure- Low blood presure- Higher heart rate- Higher heart rate

Chronic Chronic orthostaticorthostatic

- Loss of consciousness - Loss of consciousness without any sign and symptoms without any sign and symptoms

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

Occurs :- 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 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 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 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.pressure become normal or slightly higher than supine position.

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

2. Intrinsic

PATHOPHYSIOLOGY

In 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

CLINICAL MANIFESTATION OF ASTHMA

SEVERITY SEVERITY MANIFESTATIONMANIFESTATION

Mild episodeMild episode •Thickness in chestThickness in chest•Spell of couchSpell of couch•Wheezing DyspneaWheezing Dyspnea•Rise in blood pressureRise in blood pressure•Rise in heart rateRise in heart rate

Severe episodeSevere episode •Intense dyspnea and orthopneaIntense dyspnea and orthopnea•Cynosis of mucous membranesCynosis of mucous membranes•PerspirationPerspiration•Flushing of faceFlushing of face•Use of accessory muscle of respirationUse of accessory muscle of respiration•FatigueFatigue•Mental confusionMental confusion

Status asthamaticusStatus asthamaticus

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

INVESTIGATIONINVESTIGATION

1.1. Lung function testsLung function tests

2.2. PEFRPEFR

3.3. Histamine inhalationHistamine inhalation

4.4. Peripheral bloodPeripheral blood

5.5. Skin testsSkin tests

MANAGEMENTMANAGEMENT

MANAGEMENT:-MANAGEMENT:-1.1.Terminate all dental treatment.Terminate all dental treatment. Sitting positionSitting position2.2.Monitor vital signMonitor vital sign3.3.Bronchodilator by spray Bronchodilator by spray Meteprotereral Meteprotereral Isoproterenal Isoproterenal EpinephrineEpinephrine4.Administer O24.Administer O2

Signs and symptoms relieved Continues. Monitor during recovery Give epinephrine 0.3ml of DiscontinueanyIVline 1:10000IM/SC start IV & drip of crystalloid provide no dental tretment solution. until patient’s physian approves. 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.

HYPERVENTILATION SYNDROMEHYPERVENTILATION SYNDROME

Hyper ventilation is defined as ventilation inexcess of that require to maintain Hyper ventilation is defined as ventilation inexcess of that require to maintain normal blood PaConormal blood PaCo2 2 & PaO& PaO22. It may be produced by an incerase in either the . It may be produced by an incerase in either the frequency of depth of respiration or by a combination of two.frequency of depth of respiration or by a combination of two.

CausesCauses

1.1. AnxietyAnxiety

2.2. PainPain

3.3. Metabolic acidosisMetabolic acidosis

4.4. Drug intoxicationDrug intoxication

5.5. HypercapniaHypercapnia

6.6. CirrhosisCirrhosis

7.7. Organic CNS diseaseOrganic CNS disease

CLINICAL MANIFESTATIONCLINICAL MANIFESTATION

1.1. CardiovascularCardiovascular

• PalpitationsPalpitations

• TachycardiaTachycardia

• Precordial discomfortPrecordial discomfort

2.2. NeurologicalNeurological

• DizzinessDizziness

• LightheadednessLightheadedness

• Numbness and tingling of Numbness and tingling of extremitiesextremities

• Tetany (rare)Tetany (rare)

• ConvulsionConvulsion

3.3. RespiratoryRespiratory

• Shortness of breathShortness of breath

• Chest painChest pain

4.4. MusculoskeletalMusculoskeletal

• Muscle pain and crampMuscle pain and cramp

• TremorsTremors

• StiffnessStiffness

• TetanyTetany

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

Signs and symptoms of hyperventilation may be due to :Signs and symptoms of hyperventilation may be due to :

1.1. Respiratory alkslosisRespiratory alkslosis

2.2. Increased blood level of cathecolaminesIncreased blood level of cathecolamines

3.3. Decreased in level of circulating ionized calciumDecreased in level of circulating ionized calcium

MANAGEMENT :-MANAGEMENT :-•1.1. Terminate all dental procedures and Terminate all dental procedures and remove any foreign body from the mouthremove any foreign body from the mouth•2.2. Patient in upright positionPatient in upright position•3.3. Attempt to verbally calm the patientAttempt to verbally calm the patient•4.4. Have the patient breathe CO2 – Have the patient breathe CO2 – enriched air such as in and out of paper bag. enriched air such as in and out of paper bag. •5.5. If symptoms persist , administer If symptoms persist , administer diazepam –10mg IM/IV untill anxiety relieved.diazepam –10mg IM/IV untill anxiety relieved.•6.6. Monitor vital signsMonitor vital signs•7.7. perform all further dental surgery using perform all further dental surgery using anxiety reducing measures. anxiety reducing measures.

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

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

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

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

Occasionally the foreign object is aspirated into larynx, where in Occasionally the foreign object is aspirated into larynx, where in lightly sedated/ non sedated patient violent coughing will ensue. lightly sedated/ non sedated patient violent coughing will ensue.

- Patients can still talk & breathe.- Patients can still talk & breathe. If larger objects are aspirated, it obstructs the airway & becomes If larger objects are aspirated, it obstructs the airway & becomes

lodged in such away that coughing is ineffectivelodged 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 symptoms persist NO symptoms 2. Place patient in supine position -Heimlich maneuver. Observe 3. Begin abdominal thurst -Administer O2 for one

followed by turning patient on side - summon medical hour. & using finger to sweep oral assistance. cavity for foreign object . - Monitor vital signs 4. Attempt to ventilate - Transport to emergency care. Able ventilate Unable to ventilate Start BLS Administer O2 Repeat step 3&4 Transport to Laryngoscopy Emergency. Cricothyrotomy.

ANAPHYLAXISANAPHYLAXIS

• Anaphylaxis is the classical type-I immediate Anaphylaxis is the classical type-I immediate hypersensitivity reaction.hypersensitivity reaction.

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

PRIMARY AND SECONDARY REACTIONS OF ANAPHYLAXIS

1.1. SkinSkin: -: - Intense itchingIntense itching FlushingFlushing ConjunctivitisConjunctivitis PruritusPruritus UrticariaUrticaria ErythemaErythema2.2. Gastrointestinal and Gastrointestinal and

genitourinarygenitourinary Abdominal crampAbdominal cramp Nausea & vomitingNausea & vomiting Fecal and urinary Fecal and urinary

incontinenceincontinence

3.3. RespiratoryRespiratory Feeling of tightness in the chestFeeling of tightness in the chest CoughCough WheezingWheezing DyspneaDyspnea CynosisCynosis Laryngeal edemaLaryngeal edema4.4. CardiovascularCardiovascular PallorPallor PalpitationPalpitation TachycardiaTachycardia HypotensionHypotension Cardiac DysrhythmiaCardiac Dysrhythmia Loss of consciousnessLoss of consciousness Cardiac arrestCardiac arrest

PATHOPHYSIOLOGY OF ANAPHYLAXISPATHOPHYSIOLOGY OF ANAPHYLAXIS

Pathophysiology of anaphylaxis is divided in to two Pathophysiology of anaphylaxis is divided in to two phasephase

1.1. Sensitizing phase.Sensitizing phase.

2.2. Challenging phase.Challenging phase.

1.1. Sensitizing phase.Sensitizing phase.

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

2.2. Challenging phaseChallenging phase

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

CHEMICAL MEDIATORS OF ANAPHYLAXISCHEMICAL MEDIATORS OF ANAPHYLAXIS

• Primary mediatorsPrimary mediators

• HistamineHistamine

• SerotoninSerotonin

• Eosinophil chemotatic factor of anaphylaxisEosinophil chemotatic factor of anaphylaxis

• Slow reacting substance of anaphylaxisSlow reacting substance of anaphylaxis

• Secondary mediators of anaphylaxisSecondary mediators of anaphylaxis

• These includes two groups of compoundsThese includes two groups of compounds

Lipid mediatorsLipid mediators

CytokinesCytokines

Lipid mediatorsLipid mediators

• Leucotrines CLeucotrines C44 & D & D55

• Prostagladin DProstagladin D22

• Platelet activating factor.Platelet activating factor.

CytokinesCytokines

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

DIAGNOSISDIAGNOSIS

1.1. Skin testSkin test: -: -

• The characteristic skin response in ‘Wheal & Flare’The characteristic skin response in ‘Wheal & Flare’

• The skin response takes 5-15 mins to develop and may persist for The skin response takes 5-15 mins to develop and may persist for 30 mins.30 mins.

• In skin test 0.02-0.03 ml of allergen injected SC.In skin test 0.02-0.03 ml of allergen injected SC.

• Skin test is evaluated by the size of the whealSkin test is evaluated by the size of the wheal

• Normally 4*4 mm wheal in adult and 3*3 mm wheal in children Normally 4*4 mm wheal in adult and 3*3 mm wheal in children can be considered a positive response to skin testcan be considered a positive response to skin test..

2.2. Patch testPatch test: -: -

• This test include application of a patch of 10mml on 2.5cmThis test include application of a patch of 10mml on 2.5cm22 gauze that stays gauze that stays on the skin for 2 days.on the skin for 2 days.

• After 2 days biopsy is taken from that area.After 2 days biopsy is taken from that area.

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

First-line therapyFirst-line therapy

• Airway maintenanceAirway maintenance

• EpinephrineEpinephrine: -: - SC: 0.01 mL/kg, to maximum of 0.3 to 0.5 SC: 0.01 mL/kg, to maximum of 0.3 to 0.5 mL, of 1:1,000 aqueous solution (1 mg/mL)mL, of 1:1,000 aqueous solution (1 mg/mL)

• FluidFluidss: -: -5% human albumin solution, 5% human albumin solution, oror 5% dextrose in 5% dextrose in 0.5N saline solution or lactated Ringer's injection.0.5N saline solution or lactated Ringer's injection.

Second-line therapySecond-line therapy

• AntihistaminesAntihistamines : -: -Antihistamines are useful as second-line Antihistamines are useful as second-line therapy when a prolonged course is suspected. Diphenhydramine therapy when a prolonged course is suspected. Diphenhydramine hydrochloride can be given orally, intramuscularly, or intravenously at 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.a dose of 1 mg/kg up to a maximum of 50 mg every 6 hours.

• Corticosteroids Corticosteroids : -Hydrocortisone 100mg I.V.: -Hydrocortisone 100mg I.V.

• Bronchodilators Bronchodilators : -Salbuterol,IV aminophylline 5 – 6mg/kg over : -Salbuterol,IV aminophylline 5 – 6mg/kg over 20 mins20 mins

ACUTE ADRENAL INSUFFICIENCYACUTE ADRENAL INSUFFICIENCY The adrenal cortex produces and secretes over 30 steroid The adrenal cortex produces and secretes over 30 steroid

hormons most of which lake any identifiable biologic activity.hormons most of which lake any identifiable biologic activity.

Cortisol is one of the most important product of adrenal cortex it Cortisol is one of the most important product of adrenal cortex it is consider as life saving hormone as its wide spread effectis consider as life saving hormone as its wide spread effect

Hyposecretion of cortisol may produce life threatening situation.Hyposecretion of cortisol may produce life threatening situation.

There are two types of adrenal insufficiencyThere are two types of adrenal insufficiency

1.1. Primary adrenal insufficiencyPrimary adrenal insufficiency

2.2. Secondary adrenal insufficiency.Secondary adrenal insufficiency.

PREDISPOSING FACTORSPREDISPOSING FACTORS

Major predisposing factor in all type of adrenal insufficiency is lack of gluco-Major predisposing factor in all type of adrenal insufficiency is lack of gluco-corticsteroid hormone which develop through several mechanisms.corticsteroid hormone which develop through several mechanisms.

1.1. Following sudden withdrawal of steroid hormones in pt. who has primary Following sudden withdrawal of steroid hormones in pt. who has primary adrenal insufficiencyadrenal insufficiency

2.2. Following sudden withdrawal in a pt. with normal adrenal cortices but with a Following sudden withdrawal in a pt. with normal adrenal cortices but with a temporary insufficiency resulting from cortical supression by exogenous temporary insufficiency resulting from cortical supression by exogenous corticosteroid administrationcorticosteroid administration

3.3. Following stress such as physiologic & psycologicFollowing stress such as physiologic & psycologic

4.4. Following bilateral adrenalectomy or removal of functioning adrenal tumourFollowing bilateral adrenalectomy or removal of functioning adrenal tumour

5.5. Sudden destruction of pituitary gland.Sudden destruction of pituitary gland.

6.6. Following injury to the both adrenal gland by trauma, harmorrhage, infection, Following injury to the both adrenal gland by trauma, harmorrhage, infection, thrombosis or surgery. thrombosis or surgery.

CLINICAL MANIFESTATIONCLINICAL MANIFESTATION

1.1. Mental confusionMental confusion

2.2. Muscle weaknessMuscle weakness

3.3. Intense pain in abdomenIntense pain in abdomen

4.4. HypoglycemiaHypoglycemia

5.5. Extreme fatigueExtreme fatigue

6.6. Nausea & vomitingNausea & vomiting

7.7. HypotensionHypotension

8.8. Syncopal episodeSyncopal episode

9.9. ComaComa

10.10.HyperpigmentationHyperpigmentation

11.11.Loss of weightLoss of weight

12.12.Craving for salt and waterCraving for salt and water

PATOPHYSIOLOGYPATOPHYSIOLOGY

pathogenesispathogenesis Four Stages in Adrenal Four Stages in Adrenal InsufficiencyInsufficiency1.High plasma renin, low 1.High plasma renin, low aldosteronealdosterone2. Impaired cortisol response to 2. Impaired cortisol response to ACTH stimulationACTH stimulation3. Increased morning ACTH w/ 3. Increased morning ACTH w/ normal cortisolnormal cortisol4.Low morning serum cortisol4.Low morning serum cortisolTherefore, almost complete adrenal Therefore, almost complete adrenal destruction has occurred by the time destruction has occurred by the time low cortisol levels developlow cortisol levels develop

MANAGEMENTMANAGEMENT

1.1. Treminate all the treatment.Treminate all the treatment.

2.2. Position the pt. (Supine)Position the pt. (Supine)

3.3. Administer OAdminister O22

4.4. 100 mg Hydrocortisone IV over 30 seconds100 mg Hydrocortisone IV over 30 seconds

5.5. Establish IV line, IV infusion of 5% dextrose + 100mg of Establish IV line, IV infusion of 5% dextrose + 100mg of hydrocortisone over the period of 2 hrshydrocortisone over the period of 2 hrs

6.6. For severe hypotension administer 0.3 to 0.5 mg epinephrine IM or For severe hypotension administer 0.3 to 0.5 mg epinephrine IM or IVIV

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 - Patients at risk are generally those who take atleast 20 mg of corticosteroid daily for atleast 2 weeks any time during the corticosteroid daily for atleast 2 weeks any time during the year preceeding planned surgical procedure. year preceeding planned surgical procedure. If adrenal suppression is suspected. If adrenal suppression is suspected. 60 mg of hydrocortisone presugically ,60 mg of hydrocortisone presugically ,40mg the first 2 days after surgery ,40mg the first 2 days after surgery ,20 mg the next 3 days after surgery20 mg the next 3 days after surgery

DIABETES MELLITUSDIABETES MELLITUS

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

Predisposing factorsPredisposing factors

1.1. Genetic predispositionGenetic predisposition

2.2. Primary destruction of islets of langerhans in the pancreas Primary destruction of islets of langerhans in the pancreas causeed by inflammation, cancer or surgerycauseed by inflammation, cancer or surgery

3.3. Endocrine condition such as hyperpituitarism or hyperthyrodismEndocrine condition such as hyperpituitarism or hyperthyrodism

4.4. Administration of steroids. Administration of steroids.

A metabolic disease in which the patient’s long term prognosis seems dependent

upon keeping serum glucose levels close to normal.

- An untreated insulin dependant diabetic constantly runs the risk of developing

ketoacidosis

-However a common situation the diabetic patients encounter in a dental setting is

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 insulinDecreasing 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 Moderate Severe Hunger Tachycardia Hypotension Nausea Perspiration unconsciousness Mood changes Pallor seizures Weakness Behavioral Change (Uncooperativeness confusion)

MANAGEMENT :- Terminate all dental treament.

Mild Moderate - Administer glucose source - Monitor vital signs sugar/fruit juice -Administer glucose source. - Monitor vital signs (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: CHEST DISCOMFORT: The appearance of chest discomfort in a patient who may The appearance of chest discomfort in a patient who may have ischaemic heart disease in peri operative calls for rapid have ischaemic heart disease in peri operative calls for rapid identification of etiology so that appropriate measures can be identification of etiology so that appropriate measures can be taken. taken.

Clinical Manifestations of chest pain caused by myocardial ischaemia Clinical Manifestations of chest pain caused by myocardial ischaemia or infarctions:-or infarctions:-

Discomfort described by patient as being , Discomfort described by patient as being , 1.1. Squeezing, bursting , pressing, burning , choking &/ or crushing Squeezing, bursting , pressing, burning , choking &/ or crushing

in nature (not sharp/stabbing)in nature (not sharp/stabbing) 2.2. Substernally located → radiation to left shoulder, arm and /or Substernally located → radiation to left shoulder, arm and /or

left side of neck& mandible. left side of neck& mandible. 3.3. Associated with exertion, heavy meal , anxiety.Associated with exertion, heavy meal , anxiety. 4.4. Relieved by vasodilators such as nitroglycerine or rest ( in Relieved by vasodilators such as nitroglycerine or rest ( in

angina) angina) 5.5. Accompanied by dyspnoea, Accompanied by dyspnoea,

nausea,weakness,palpitations,perspirationnausea,weakness,palpitations,perspiration

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

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 continues 3 minutes after TNG

Assume angina pectoris Second TNG dose

was present Monitor vital signs

taper O2 over 5 min 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,In that case,1.1. Summon medical assistance Summon medical assistance 2.2. Start Iv line with drip of crystalloid solution.Start Iv line with drip of crystalloid solution.3.3. If severe discomfort is present morphine sulfate 2 mg If severe discomfort is present morphine sulfate 2 mg sc/Iv every 3 minsc/Iv every 3 min4.4. Prepare for transport to emergency care facilityPrepare for transport to emergency care facility

LOCAL ANESTHETIC TOXICITY:- LOCAL ANESTHETIC TOXICITY:-

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

Prevention:-Prevention:- - Least effective dose to be given - Least effective dose to be given - Patients age, lean body mass, liver function, and history of problems - Patients age, lean body mass, liver function, and history of problems

with local anesthetics must be considered .with local anesthetics must be considered . - Manner of administration -slow & intra vascular injection should be - Manner of administration -slow & intra vascular injection should be

avoided.avoided. - Use of Vasoconstrictors to slow the entry of local anesthetic into the - Use of Vasoconstrictors to slow the entry of local anesthetic into the

blood. blood. → → Should be remembered that, topical use of LA in wounds/on mucosal Should be remembered that, topical use of LA in wounds/on mucosal

surfaces allows rapid entry of local anesthetics into the systemic surfaces allows rapid entry of local anesthetics into the systemic circulation. circulation.

→ → Choice of local anesthetics – Local anesthetics vary in their lipid Choice of local anesthetics – Local anesthetics vary in their lipid solubility vasodilatory properties , protein binding and inherent toxicity. solubility vasodilatory properties , protein binding and inherent toxicity.

So the dentist should be knowledgeable about various local So the dentist should be knowledgeable about various local anaesthetics. anaesthetics.

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

Tremors, headache, dizziness, Supine position Blurred vision Drowsiness monitor vital signs , Administer O2 observe in office for 1hr.

Severe Toxicity Seizure ,cardiac dysrrhythmia Supineposition. or arrest 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