Steroids in oral and maxillofacial surgery

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  • "impetus=Something that incites; a stimulus.
  • It has been almost 60 years since corticosteroids were first recognized for their anti-inflammatory and immunosuppressive properties, initially in rheumatologic diseases. The beneficial effects of steroids in rheumatoid arthritis were described in 1949 by Philip S. Hench and colleagues, a discovery for which he received (together with Edward C. Kendall and Tadeus Reichstein) the Nobel Prize in medicine in 1950.1,2
  • The adrenal glands produce three major classes of hormones, each of which aid in dealing with the multitude of small and large stresses faced by animals and people almost daily. There is no doubt that at least two of these groups - glucocorticoids and mineralocorticoids - are necessary for life.
  • DHEA IS A METABOLIC INTERMEDIATE IN SYNTHESIS OF ANDROGENS.
  • cycles of cortisol levels are found in several animal species, including humans.[3] In species that exhibit such cycles, different timing of diurnal maxima and minima has been observed, not only in different species[3] but also, in some cases, within the same species.[13][14][15]In humans, the amount of cortisol present in the blood undergoes diurnal variation; the level peaks in the early morning (approximately 8 am) and reaches its lowest level at about midnight-4 am, or three to five hours after the onset of sleep. Information about the light/dark cycle is transmitted from the retina to the paired suprachiasmatic nuclei in the hypothalamus. This pattern is not present at birth; estimates of when it begins vary from two weeks to nine months of age.[16]Changed patterns of serum cortisol levels have been observed in connection with abnormal ACTH levels, clinical depression, psychological stress, and physiological stressors such as hypoglycemia, illness, fever, trauma, surgery, fear, pain, physical exertion, or temperature extremes. Cortisol levels may also differ for individuals with autism or Asperger's syndrome.[17]
  • Cortisol also exerts permissive actions. This refers to the fact thatthe action of some hormones requires the presence of cortisol. For example,cortisol must be present in order for glucagon and catecholamines to exert their calorigenic action, and for catecholamines to exert their lipolytic effect.
  • Because-peripheral adipocytes are less sensitive to insulin,corticosteroids action predominate,whereastruncaladipocytes respond mainly to enhanced insulin levels under the influence of corticosteroids.
  • Cortisol maintains the responsiveness of vascular smooth muscle to catecholamines and therefore participates in blood pressure regulation. This is another example of a permissive action of cortisol. In adrenal insufficiency, vascular smooth muscle becomes unresponsive to catecholamines. The decreased responsiveness, together with the associated hypovolemia caused by mineralocorticoid deficiency, can result in severe hypotension.
  • Corticosteroids inhibit phospholipase A2* This leads to reduction in PG levels in the stomach* Cytoprotective effect of PGs is thereforelost peptic ulcer.(this is not due to destruction of these cells but due to their sequestration in tissues)* Misoprostol ( A prostaglandin E1, analogue) may be used to replenish the depleted stomach PGS.* Misoprostol causes a) diarrhoea. b) abortion
  • suppresses phospholipase , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events (epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, etc.).
  • cortisol-induced collagen loss in the skin is ten times greater than in any other tissue
  • Corticosteroidspenetrate cells and bind to a high affinity cytoplasmic receptor protien-> a structural change occurs in the steroid receptor complex that allows its migration into the nucleus and binding to specific sites on the chromatin->trancription of specific m-RNA->regulation of protien synthesis .
  • Like most steroids, cortisol is metabolized in the liver. It has a half life of 60-90 minutes in the circulation. Most of the cortisol is reduced to dihydrocortisol and then to tetrahydrocortisol which is conjugated to glucuronic acid . Some cortisol is converted to cortisone.Note that cortisone is an active glucocorticoid but that it is formed in the liver, not in the adrenal. The tetrahydroglucuronide derivatives of cortisol and cortisone are water soluble and are excreted in the urine.Oral boiavailabilty of synthetic corticoids is high.
  • Pulse therapy with high dose methy-pred (1 g infused i.v. every 6-8 weeks)in autoimmune diseases.with good results and minimal suppression of pituitary-adrenal axis.the initial effect of this is due to its antiinflammatoryaction,while long term benefit is due to temporary switchin of immunodamaging process as a cosequence of lymphopenia and deceased IG synthesis.
  • Not used clinically coz of low oral bioavailability and difficulty in regulating doses.
  • as in severe TB,severeleprareaction,pneumoocystiscarinii in AIDS patient.
  • Dexa used to test hpa.at dose which donot contribute to steroid metabolite in urine.responsiveness tested by measuring daily urinary steroid metabolite excretion.
  • Osteoporosis arrested by ca supplement,vit d ,bisphosphonate,estrogen-androgen replacement)
  • Moderate dose of short acting steroids given at 48 hrs interval did not cause HPA suppresion.whereas same total amount given in 4 divided 12 hourly doses pruduced marked HPA depression.alternate day therapy resultsnin less immunosupression-lower risk of infection.the long acting steroids (dexa) are not suitable for alternate day therapy.onlyprolem with alternate day therapyare incapacitated on the “off”day.
  • 1. Adams and Siderius ' have reported on five patients with postoperative shock in whom they felt the diagnosis of adrenal insufficiency was justified. one patient had persistent hypotension and tachycardia.In the immediate postoperative period the hypotension became severe, despite adequate blood, fluid, and electrolyte therapy. Levarterenol (Levophed) bitartrate was given continuously but was ineffective. On the third postoperative day hydrocortisone sodium succinate (Solu-Cortef) was given intravenously, and the blood pressure rose sharply and gradually stabilized. The patien received a total of 250 mg. on the third day and 200 mg. on the fourth day. No levarterenol was required. The patient recovered and was discharged on the 14th postoperative day.
  • Patients on steroids who present for surgery may be at increased risk of complications because of:The adrenal suppression caused by steroid therapy.This often poses the greatest risk and deserves particular attention. The disease or condition which required them to take steroids. Corticosteroids are used in a wide variety of conditions. Some of these may also have attached risks for anaesthesia (those for example affecting lungs, neck joints or drug metabolism).Long-term and other side-effects of steroid therapy.There are preoperative, perioperative and postoperative factors to be considered when assessing and managing these risks.
  • Hempenstallet al. compared cortisollevels in patients having either a generalanaesthetic or sedation for surgical removal of third molar teeth. Cortisol levels remained unchanged in the sedation group but rose significantly after surgery in patients who had a general anaesthetic
  • Steroids in oral and maxillofacial surgery

    1. 1. corticoSTEROIDSShivani gaba Jr-ii,omfs 1
    2. 2. Endocrine system maintains homeostasis  The concept that hormones acting on distant target cells to maintain the stability of the internal milieu was a major advance in the historical events of physiological understanding of human body. Ernest Henry Starling (1866-1927)was the first to use the term hormone(from Greek ὁρμή, "impetus") 2
    3. 3. 3
    4. 4. This is especially important in oral surgery because many of the patients attending the our clinics face stressful situations. Awareness is therefore necessary of -the risks and difficulties that may arise during the surgical management of patients with endocrine disorders; and the most common oral manifestations. 4
    5. 5. objectives History Steroids physiology Actions Pharmokinetics Preparations Therapeutic principals and uses Steriods withdrawal Surgical management & Adrenal crisis Cushing syndrome Misuse From literature 5
    6. 6. Steroids 6
    7. 7. History of steroid therapy It has been almost 60 years since corticosteroids were first recognized for their anti-inflammatory and immunosuppressive properties, initially in rheumatologic diseases( in 1949) by Philip S. Hench and colleagues, a discovery for which he received (together with Edward C. Kendall and Tadeus Reichstein) the Nobel Prize in medicine in 1950. Currently,corticosteroids are the drugs with one of the broadest specturm of clinical utility. 7
    8. 8. E D W A RD C. KE N D A L L The development of cortisone as a therapeutic agent Nobel Lecture, December 11, 1950 From the time, ages ago, when cortisone was first made in the adrenal cortex it has continued to serve as a powerful agent in health and disease.. What physiologic processes are modified by cortisone and how this influence is exerted are matters still locked within this hormone of the adrenal cortex. Said Shakespeare’s soothsayer, "In Nature’s infinite book of secrecy a little I can read." 8
    9. 9. corticosteroids  The term “corticosteriods”(also called simply steroids) refers both -to the hormones produced in outer layer(cortex) of adrenal glands and -to the modified forms of these hormones that are used as drugs.  Despite the name , corticosteroids should not be confused with anabolic steroids , substances that mimic the virilizing effects of testosterone and are some times used illegally by athletes to build up muscle mass. 9
    10. 10. Adrenal glands  When you think about the adrenal glands, you should think about stress. Stress can take many forms: taking an examination, recovering from a broken bone, running away from an invading army, starvation. For human males, there is even considerable stress associated even with shopping . 10
    11. 11.  The two adrenal glands are located immediately anterior to the kidneys, encased in a connective tissue capsule and usually partially buried in an island of fat. Their combined weight is about .01-.02% of total body weight in both males and females.  Inspection of a mammalian adrenal gland that has been sectioned reveals two distinct regions.  An inner medulla, which is a source of the catecholamines epinephrine and norepinephrine. The chromaffin cell is the principle cell type. The medulla is richly innervated by preganglionic sympathetic fibers and is, in essence, an extension of the sympathetic nervous system.  An outer cortex, which secretes several classes of steroid hormones (glucocorticoids and mineralocorticoids, plus a few others). Histologic examination of the cortex reveals three concentric zones of cells that differ in the major steroid hormones they secrete. 11
    12. 12. 12
    13. 13. 13
    14. 14. Steroids-biosynthesis Adrenal cortex makes and secretes over 30 different steroid hormones (collectively called corticosteroids).Corticoids are 21 carbon compounds having a cyclopentanoperhydro-phenanthene(steroid) nucleus. Since adrenal cortical cells store only minute quantity of hormone ,rate of release is governed by the rate of biosynthesis. 14
    15. 15. 15
    16. 16. Hypothalamic-pituitary- adrenal axis  The hypothalamic-pituitary-adrenal (HPA) axis is a feedback loop that includes the hypothalamus, the pituitary and the adrenal glands. The main hormones that activate the HPA axis are corticotropin-releasing factor (CRF), arginine vasopressin (AVP) and adrenocorticotropin hormone (ACTH). The loop is completed by the negative feedback of cortisol on the hypothalamus and pituitary. 16
    17. 17. CORTISOL ACTH CRH STRESS: Physical stress Emotional stress Hypoglycemia Cold exposure Pain Adrenal Cortex Anterior Lobe of Pituitary Gland Hypothalamus 17
    18. 18. Diurnal rhythm  ACTH is secreted in irregular pulses throughout the day which cause parallel increases in plasma cortisol . Both the frequency and the amplitude of the pulses are the greatest in the early morning.  This early morning increase in ACTH release is initiated by the release of CRH (corticotropin releasing hormone) and starts approximately a couple of hours before waking.  The lowest levels of ACTH in blood occur just before or after falling asleep. This results in the characteristic diurnal rhythm in ACTH and cortisol secretion 18
    19. 19. ACTIONS . Cortisol is one of the few hormones essential for life. Adrenalectomy in humans is always fatal unless glucocorticoids are administered.Exactly why adrenal insufficiency results in death is not well understood, but in view of the widespread actions of the glucocorticoids, it is not surprising that they are needed for life 19
    20. 20. Pharmacological Actions Direct Actions Permissive Actions •Lipolytic effects •Effect on BP •Effect on bronchial muscles (e . g . sympathomimetic amine) 20
    21. 21. Pharmacological Actions 1. Mineralocorticoid actions 2. Glucocorticoid actions  Carbohydrate  Protein  Lipid  calcium metabolism  CVS  Skeletal muscle  CNS  Stomach  Respiratory system  lymphoid tissue and blood cells  Inflammatory responses  Immunological and allergic responses  Growth & Cell Division 21
    22. 22. 22 Mineralocorticoid Actions: Electrolyte and water balance
    23. 23. As a result, blood glucose increases(hyperglycemia,a diabetes like state). The metabolic effects of glucocorticoids may be counterbalanced by those of other hormones, particularly insulin, the secretion of which is stimulated by the rise in blood glucose 23
    24. 24. Lipid metabolism  Permissive action  Promote adipokinetic agents activity(lipolysis)  Redistribution of Fat  Moon face , fish mouth , buffalo hump 24
    25. 25. Calcium metabolism  ↓ Intestinal absorption  ↑Renal excretion  OSTEOPOROSIS-spongy bones are more sensitive(e.g., vertebrae, ribs etc) Cardiovascular system Restrict capillary permeability Maintain tone of arterioles & Myocardial contractility Na+ sensitize blood vessels to the action of catecholamines & angiotensin-(permissive role in development of hypertension ,should be used cautiously in hypertensives) Skeletal muscle Optimum level of corticosteroid is needed for normal muscular activity. Hypocorticisim : ↓ work capacity & weakness(due to hypodyanamic circulation) Hypercorticism : •excess mineralocorticoid action - hypokalemia – weakness •excess glucocorticoid action - muscle wasting & myopathy - weakness CNS Direct: Mood(mild euphoria),Behaviour,Brain excitability,High doses lower seizure threshold-cautious use in epileptics Indirect: maintain glucose, circulation and electrolyte balance 25
    26. 26. Stomach ↑ section of gastric acid &pepsin&↓ in PG levels in the stomach-- Cytoprotective effect of PG lost--result- -peptic ulcer Misoprostol ( A prostaglandin E1, analogue) may be used to replenish the depleted stomach PGS Lymphoid tissue and Blood cells •Lymphoid tissue: • ↑ rate of destruction of lymphoid cells(T cells are more sensitive than B cells) •Blood cells: ↑ number of RBCs,platlets,neutrophils in circulation. ↓ lymphocytes,eosinophils and basophils blood count come back normal after 24 hours. Inflammatory responses Irrespective of type of injury the attending inflammatory response is ↓ed.The cardinal signs of inflammation –redness,heat,swelling and pain are suppressed. In early events:↓acute inflammatory response, reduced exudation, ↓ in numbers and activity of leucocytes, ↓ in inflammatory mediators In late events:↓numbers and activity of mononuclear cells and fibroblasts, ↓ proliferation of blood vessels, less fibrosis-thus ↓ chronic inflammation but also ↓ healing 26
    27. 27. Phospholipids Arachidonic acids lipoxygenase Cycylooxygenase Leukotriene Prostaglandins, Thromboxane Prostacyclins Phospholipase A2 Lipocortin Corticosteroids 27
    28. 28. Causes greater suppression of CMI (graft rejection & delayed hypersensitivity) ↓Transplant rejection: ↓antigen expression from grafted tissues, ↓sensitisation of T lymphocytes. Which makes the basis of use in autoimmune diseases and organ transplantation. 28
    29. 29. Growth & Cell division  Delays the process of healing and scar formation.  Retards the growth of children Respiratory system •Most potent and most effective anti-inflammatory •Effects not seen immediately (delay 6 or more hrs) •Inhaled corticosteroids are used for long term control in bronchial asthma. Effects on stress ACTH and cortisol secretion are increased by stressful stimuli including surgery , trauma, pain, apprehension, infection, hypoglycemia and hemorrhage. The increase in cortisol production is necessary for survival, and stresses that are normally tolerated can become fatal in adrenal insufficiencyRapid deterioration resulting in organ damage and shock/coma/death can occur, especially in children. Cortisol response to a minor (dashed line) and major (solid line) surgery 29
    30. 30. This process takes 30-60 min.So effects of corticosteroids are not immediate ,and once the appropriate proteins are synthesized-effects persist much longer than steroid itself Mechanism of action 30
    31. 31. Metabolism:  Basal Cortisol Production = 8-25 mg/24hrs  Cortisol Production can be  6-fold in stress  Metabolism by liver enzymes  excretion by urine  plasma t1/2 of cortisol 60-90 min in circulation.  biological t1/2 is longer-effects persist long after steroid is removed from plasma. Bioavailability: Hydrocortisone undergoes high first pass metabolism,has low oral: parentral activity ratio.Oral bioavailability of synthetic corticoids is high. Transport: Transcortin 75% Albumin 5% Free form 20% 31
    32. 32. Preparations Glucocorticoids Short acting Intermediate acting Long acting Mineralocorticoids Inhalant steroids Topical steroids  SYNTHETIC STEROIDS have largely replaced the natural compound s in therapeutic use ,because they are potent,longer acting,more selective,for glucu/mineralo action and have high oral activity. 32
    33. 33. Short Acting Preparations (t1/2 < 12 h) Drug Anti- inflam. Salt retaining Preaparations & dose Cortisol 1 1.0 • 5 mg tablet , 100 mg/vial (i.m., i.v) • Topical, enema(in ulcerative colitis) Uses:for replacement therapy -20 mg morning+10 mg afternoon(oral) •shock,status ashmaticus,acute adr.insufficiency- 100mg i.v. bolus+100mg 8 hrly infusion. Cortisone 0.8 0.8 • 5 mg tablet • 25 mg/vial (i.m) Intermediate Acting Preparations (t1/2 = 12 -36 h) Prednisolone 5 0.3 • 5, 10,20 mg tablet , 20 mg/vial (i.m, intrarti) •Topical,used for allergic,inflammatory,autuimmune disease,malignancy:5-60 mg/day oral,10-40 mg i.m. intra-articular Methyl prednisolone 5 0 • 0.5, 1.0 gm inj. for i.m. or slow i.v.(4-32mg/day oral) Enema,pulse therapy in nonresponsive rh artritis,renal transplant,pemphigus Triamcinolone 5 0 • 4 mg Tab.,10, 40 mg/ml for i.m., intrarticular inj. (4-32mg/day oral,5-40 mg i.m.,intraricular) Topical33
    34. 34. Drug Anti-inflam. Salt retaining Preapartions & dose Dexamethasone 25 0 0.5 mg tab. 4mg/ml inj (i.m., i.v.),Topical used for: inflammatory and allergic conditions 0.5-5 mg/day oral,shock,cerebral edema 4-20mg/day i.v. infusion/i.m. inj. Betamethasone 25 0 0.5, 1 mg tab. 4mg/ml inj (i.m., i.v.),topical Uses:same as dexamethasone Paramethasone 10 0 2- 20 mg/day (oral) Long Acting Preparations (t1/2 > 36 h) 34
    35. 35. Mineralocorticoids - Preparations Drug Anti-inflam. Salt retaining Preapartions & dose Fludrocortisone 10 150 100 mcg tab. DOCA 0 100 10 mg /ml inj.,used occasionally for replacemen t therapy in addison’s disease2-5 mg sublingual , 10-20 mg i.m. once or twice weekly Aldosterone 0.3 3000 Not used clinically 35
    36. 36. Prednisolone 10 mg is equivalent to  Betamethasone 1.5 mg  Cortisone acetate 50 mg  Dexamethasone 1.5 mg  Hydrocortisone 40 mg  Methylprednisolone 8 mg 36
    37. 37. Replacement therapy(for endocrine diseases) Pharmacotherapy( for non-endocrine diseases) Diagnostic uses Uses of steroids therapy 37
    38. 38.  Long term use is potentially hazardous.keep dose to minimum which is found by trial & error; Needs frequent evaluation.  Single dose: No harm ,can be used to tide over mortal crisis.  Few days therapy (even high doses)unlikely to be harmful  Incidence of side effects related to duration of therapy  Use is only palliative (except replacement therapy)  infection,severe trauma or any stress during therapy:↑ dose  Abrupt cessation of prolonged high dose(>2-3 weeks) leads to adrenal insufficiency (contraindicated) 38
    39. 39. •Replacement therapy 1.Acute adrenal insufficiency:  an emergency  Hydrocortisone  Amount of fluid infused-governed by-b.p.  2.Chronic adrenal insufficiency: (addison’s disease):  Hydrocortisone given orally,Supplemented with –a mineralocorticoid (fludrocortisone)  3.Congenital adrenal hyperplasia  Familial disorder due to def.of of 21-  hydroxylase &11 -  hydroxylase enzyme.  Treatment:hydrocortisone 0.6 mg /kg/day in divided doses . 39
    40. 40. •Non-endocrine diseases 1.arthritis: rheumatoid ,osteoarthritis , rheumatic fever , gout 2.Collegen diseses:SLE,polyarteritis nodosa,dermatomyostitis,nephrotic syndrome,glomerulonephritis  May be life saving  Started with high dose-tapered to maintainance dose when remission occurs. 3.Severe allergic reactions: anaphylaxis,angioneurotic edema,urticaria,serum sickness.  Even i.v. inj takes 1-2 hours to act,So not a substitute to adr.in anaphylaxis and angioedema of larynx. 40
    41. 41. Non-endocrine diseases 4.Autoimmune diseases : Hemolytic anaemia , trombocytopenia , MS, active chronic hepatitis , myasthenia gravis. 5.Bronchial asthma:  Status asthmaticus ,Severe chronic asthma:as a supplement to bronchodilators. 6.Other lung diseases: Aspiration pneumonia,pulmonary edema ,for lung maturation in foetus ,to prevent RDS in cases of premature delivery. 7.Infective diseases : Under effective chemotherapeutic cover , corticosteroids are indicated only in serious infective diseases to tide over crisis or to prevent complication. 8.Eye diseases: Inflammatory ocular diseases-may prevent blindness. 41
    42. 42. Non-endocrine diseases 9.Skin diseases: Life saving in-pemphigus vulgaris,exfoliative dermatitis,stevens johnson sysndrome. 10.Intestinal diseases: Ulcerative colitis,crohn’disease,coeliac diseses 11.Cerebral edema: Due to tumors,tubercular meningitis,Dexa or beta-methasone preferred . 12.Malignancies: ALL,hodgkin’s,other lymphoma,secondary role in breast carcinoma,symptomatic relief in advance malignancy. 13. Liver diseases • Subacute hepatic necrosis & chronic active hepatitis: Improves survival rates • Alcoholic hepatitis: reserved for pts. with severe illness 42
    43. 43. Non-endocrine diseases 14. Shock Septicaemic shock. 15.Organ tranplant and skin allograft: High dose corticosteroids +other immunosuppressants to prevent rejection followed by low maintenance dose. 16. Miscellaneous With chemotherapy(antiemetic),Bell’s palsy,Thrombocytopenia,Spinal cord injury,Sarcoidosis ,Hypercalcemia,IBD Diagnostic Uses: Cushing’s syndrome To locate the source of androgen production in hirusitism 43
    44. 44.  Mineralocoricoids:sodium and water retention,edema,↑ b.p.  Glucocorticoids:  1.cushing habitus cutaneous atrophy occurs with topical use also.  Precipitation of diabetes.  Susceptibility to infection.(opportunistic)  Delayed healing  Peptic ulceration(silent perforation of ulcers)  Osteoporosis(spongy bones)(r/g evidence of osteoporosis – indication of withdrawal of therapy)  Posterior subcapsular cataract(in children)  Growth retardation(↓GH)  FOETAL abnormality  Psychaitric disturbances  Suppression of HPA axis 44
    45. 45. Longer the duration of therapy, slower the withdrawal Less than 1 week: withdrawal in few steps  Rapid withdrawal: 50% reduction of dose every day  Slow withdrawal: 2.5 – 5 mg prednisolone reduced at an interval of 2-3 days  Longer period & high dose:  Half the dose weekly until 25 mg prednisolone or equivalent is reached  Later reduce by about 1mg every 3-7 days. HPA axis recovery may take months or up to 2 years 45
    46. 46.  In The patients with steroids therapy for long time,the adrenal cortex atrophies and stoppage of exogenous steroids precipitates a withdrawal syndrome- Malaise,fever,weakness,pain in muscles and joints and reactivation of disease.  Subjected to stress these patients may go into acute adrenal insufficiency.  So any patient who has received >20-25 mg/day hydrocortisone or equivalent for longer than2-3 weeks should be put on a scheme of gradual withdrawal .  Such patients may need protection with steroids if a stressful situation developes upto one year after withdrawal.  If a patient on steoids develops an infection –the steroids should not be discontinued despite its propensity weaken host defence.Rather,the dose may have to be increased to meet the stress of infection. 46
    47. 47.  Use shorter acting steroids(hydrocortisone,prednisolone) at the lowest possible dose.  Use steroids for the shortest peroids of time possible.  Give entire daily dose at one time in morning.  Switch to alternate day therapy if possible.  If appropiate ,use (dermal,inhaled,ocular,nasal,rectal,intrasyno vial)prep.of steroid with poor systemic availability(beclomethasone,triamcinolone,fl uticasone) 47
    48. 48. Contraindications (relative)  Infections  Hypertension with CCF  Psychosis  Peptic ulcer  Diabetes mellitus  Osteoporosis  Glaucoma  Pregnancy : (methylprednisolone preferred)  Epilepsy  Renal failure 48
    49. 49. 1.Moonface’ – excess adipose tissue in face 2 ‘Buffalo Hump’ – excess cervical adipose tissue 3 Striae 4 Excess adipose tissue in trunk 5 Thin limbs 6 Thinning of skin on limbs 7 Bruising on extremities 8 Amenorrhea, decreased libido 9 Osteoporosis, fractures easily 10 Hirsutism 11 Acne 12 Mood swings There are no specific oral manifestations,but,though it may be hard to believe ,patients have been referred to dentists,for suspected cause of the swollen face!! Cushing syndrome-clinical features Dental management in these patients consists in ---LA is preffered for pain control. preventionof infections pathological fractures during surgical treatments complications such as hypertension,CVS problems, hyperglycemia, depression and delayed healing. Consider supplementation. 49 If the steroid dose is reduced too quickly after replacement therapy in post surgical patients with cushing syndrome,,features:lethargy,abdominal pain,hypotentionscaly desquamation of facial skin,paticularly of forehead,is a characteristic sign.
    50. 50. Adrenocortical hypofunction  1⁰-due to adrenal disesae(addision’s disease)  2⁰-following use of systemic steroids  addision;’s disease- (autoimmune)  c/f-hypotention,hypogyycemia,hyperpigmentation,vulnerable to any stress such as infection, trauma, surgery, aneasthesia, fatigue, weakness, lethargy,weigh t loss,anorexia,dizziness  Rᵪ-most patients are treated with oral hyrocortisone and fludrocortisone  Dental aspects:risk of ppt hypotensive collapse,prefer LA for pain control (over concious sedation and GA),oral hyperpigmentation 50
    51. 51. Adrenal Crisis  Life-threatening emergency characterised by collapse ,  bradycardia,hypotension,profound weakness,hypoglycemia,vomiting,and dehydration  The early indicators of an adrenal-crisis onset can be vague and non-specific.  Management:  Lay patient flat and leg raised  Give 200 mg hydrocortisone i.v. and summon medical assistance  Take blood for glucose and electrolyte estimation  Give glucose if there is hypoglycemia(25 mg orally or i.v.)  Put up an infusion of NS or glucose –saline.  Give I litre. For two hours together with 200mg hydrocortisone sodium succinate,repeating this at 4-6 hourly intervals as req. and monitor b.p.  Determine and deal with underlying cause,control of pain &infection  Steroids supplementation must be continued for 3 days after the b.p.has retuned to normal. 51
    52. 52.  Systemic steroids are often effective in the treatment of oral lesions due to noninfectious inflammatory disease.  Topical use: non-infections, ulcerative diseases in oral cavity. Inhibit the inflammatory reaction, redness and edema,  Systemic use: third molar extraction, minor and major surgery to reduce edema,pain,trismus .Temporomandibular joint disorders,oral submucous fibrosis 52
    53. 53. Surgical management of a patient on steroid therapy 53
    54. 54. Implication  Barely three years later after the discovery of steroids , Fraser and coworkers reported the death of a 34-year-old man after routine orthopedic surgery due to shock, adrenal insufficiency, and circulatory collapse. The patient had been on corticosteroids for rheumatoid arthritis, but the treatment had been stopped prior to surgery. 54
    55. 55. Surgery-activation of HPA axis  Surgery is one of the most potent stressors that can cause activation of the HPA axis. The degree of activation depends on the type and duration of surgery and anesthesia, with many other variables adding to the picture, including analgesics, antihypertensive medications, infections, and age.  The maximum stimulation of the HPA axis is occur during reversal of anesthesia and in the immediate postoperative period. 55
    56. 56. Significant hypotension??  Significant hypotension which cannot be explained by acute blood loss, myocardial infarction, anesthesia, drugs, or electrolyte imbalance should suggest the possibility of an acute adrenal insufficiency. This is especially true if the blood pressure does not respond promptly to blood transfusions or vasopressors.  It is suggested that an increase in capillary resistance and potentiation of the effect of vasoconstrictors on blood vessels may be factors in the blood pressure response to adrenal corticosteroids. Adams, R., and Siderius, N.: Postoperative Acute Adrenal Cortical Insufficiency, J. A. M. A. 165:41-44 (Sept. 7) 1957 56
    57. 57. SUPPLEMENTATION  Lack of increase in cortisol production during stress would cause the host to succumb to it. On the other hand, too much cortisol would be detrimental, causing increased tissue breakdown, poor wound healing, and immunosuppression.  Given this background, it is clear that any patient who has inadequate cortisol production in response to surgical stress will fare poorly in such a situation. This patient will need to be recognized, and his acute steroid requirement will have to be estimated and supplemented. 57
    58. 58. Preoperative considerations Adrenocortical function may be suppressed if:  The patient is currently on daily systemic corticosteroids at doses above 7.5 mg prednisolone(or equivalent)  Cortisteroids has been taken regularly during the past 30 days.  Corticosteroids have been taken for more than one month during past one year.  Although the evidence for the need of steroid cover may be questionable,medicolegal and other considerations suggest that one should act on the side of caution and fully inform and discuss with patient,take medical advice in case of doubt,give a steroid cover unless confident that collapse is unlikely. 58
    59. 59. Intraoperative consideration  B.p. must be carefully watched during surgery and especially during recovery.,and steroid supplementation must be given if b.p. starts to fall.  Drugs especially sedative and GA ,are a hazard and it is extremely important to avoid hypoxia,hypotention and haemorrhage  Patient may also require special management as a result of diabetes,hypertention ,poor wound healing and infections. 59
    60. 60. Procedure No steroids for previous 12 months Steroids taken during previous 12 months Steroids currently taken Conservative dentistry or dentoalveolar surgery ↓LA No cover required Give usual oral steroids dose in morning or hydrocortisone 25- 50mg i.v. preop Double oral steroids dose in morning or hydrocortisone 25- 50 mg i.v. preop,continue normal steroid medication postop Intermediate surgery(multiple extractions,or surgery ↓GA) Consider cover if large doses of steroids were given Give usual steroids dose in morning +hydrocortisone 25- 50 mg i,.v. preop + i.m. 6 hourly for 24 h Double oral steriod dose in morning +hydrocortisone 25- 50mg i.v.preop + i.m.6 hourly for 24 h,then continue normal med. Maxillofacial surgery or trauma Consider cover if large doses were given Same+i,.m 6 houly for 72 h Same +i.m. 6 hourly for 72 h+normal thereafter 60
    61. 61. ROUTINE DENTAL PROCEDURES REMEMBER:  Conducting treatment in the morning.  Control of anxiety and emotional stress.  Use long-acting anesthetics.  Treatment of postoperative pain.  Minimum use of NSAIDs  Aseptis surgery ,Antibiotic prophylaxis  Prevention of iatrogenic fracture during surgery .  topical steroids for use in mouth predispose to oral candidiosis. 61
    62. 62. From litreture Gersema L, Baker K. Use of corticosteroids in oral surgery.J Oral Maxillofac Surg. 1992 Mar;50(3):270- Perioperative use of corticosteroids has been advocated for reduction of pain, edema, and trismus following oral surgical procedures. It was demonstrated that corticosteroids reduced the amount of inflammation , especially edema. No significant adverse reactions were noted. Based on these studies, the use of perioperative corticosteroids appears to be a safe and rational method of reducing postoperative complications following the removal of impacted third molars 62  Oral submucous fibrosis: etiology, pathogenesis, and future researchR. Rajendran1. Bulletin of the World Health Organization, 1994, 72 (6): 985-996  Immunomodulatory drugs and systemic application of glucocorticoids and placental extract are commonly used. By opposing the action of soluble factors released by sensitized lymphocytes following activation by specific antigens, glucocorticoids act as immunosuppressive agents . These also prevent or suppress inflammatory reactions, thereby preventing fibrosis by decreasing fibroblastic proliferation and deposition of collagen.
    63. 63. From litreture 63 Emerging intra-articular drug delivery systems for the temporomandibular joint. Mountziaris PM, Kramer PR, Mikos AG.Methods. 2009 Feb;47(2):134-40. Intra-articular injections of corticosteroids and hyaluronic acid are currently used to treat chronic painof TMJ.The most common treatment strategy is either a single injection or a series of two injections spaced 14 days apart .A single corticosteroid injection is beneficial for patients with severe TMJ pain, while further injections do not provide added pain relief, and may increase the risk of joint degeneration and other complications Kondoh T et al ..Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Dec;98(6):651-6 Aim was to compare the the clinical outcome of intra-articular irrigation and corticosteroid injection into the superior joint compartment (SJC) of patients and conventional closed reduction with IMF with fresh mandibular condyle fractures. Clinical outcome was determined by clinical examination of jaw motion, joint pain, and occlusal changes. It was concluded that the modified treatment protocol involving intra-articular corticosteroid injection is a more effective and quick-acting modality than conventional closed reduction with IMF for functional recovery and control of clinical symptoms of patients with unilateral fresh condylar fractures
    64. 64. Say “NO” to the mis-use!! A patient consults a general dental practitioner for burning sensation in the mouth The dentist looks into the mouth, finds red patches on the buccal mucosa and tongue prescribes a topical steroid. Within few days the burning sensation increases manifold times making life miserable for the patient Such events are not uncommon in today’s practice. This patient probably had oral candidiasis predisposed by some underlying factor (e.g. diabetes). The use of a steroid further increased the immune suppression locally, resulting in the flare up of the fungal infection This is a clear case of misuse of steroid 64
    65. 65. USE TOPICAL STEROIDS WISELY!! Althoughthe practitioners have learnt (as students) that steroids are “double edged weapons” many of them consider steroids as panacea Steroids are used by every practitioner irrespective of their speciality. Steroids can be administered in various forms, but its use or misuse is generally restricted to topical preparations in dentistry(KENACORT) Some general practitioners use them for any ulcer or even an area of erythema in the oral cavity. Unfortunately these preparations can also be bought over the counter .... It doesn’t end there. The patient uses the preparation till he feels better and stops or keeps using it for an unlimited period without consulting the dentist again To make the situation worse, the patient recommends its use to anyone who has an ulcer in the mouth. Although nothing catastrophic is going to happen, such misuse for prolonged periods can result in unexpected and unwanted effects and delay in the correct diagnosis and proper management. Somasundaram Elangovan,A RETHINK ON THE USE OF TOPICAL STEROIDSe-Journal of Dentistry July - Sep 2011 Vol 1 Issue 3 65
    66. 66. conclusion In Addison’s disease: We must conduct treatment in the morning and control of anxiety. In patients with corticotherapy, we must evaluate the necessity to administer additional corticosteroids. In Addisonian crises: we should interrupt dental procedure. Unexplained hyponatremia and hyperkalemia in the setting of hypotension unresponsive to catecholamine and fluid administration… should receive 100mg hydrocortisone intravenously In hyperadrenocorcism: we must prevent infection and pathological fractures. 66
    67. 67. •Jabbour SA. Steroids and the surgical patient. Med Clin North Am. 2001 Sep;85(5):1311-1317. •Hume DM, Bell CC, Bartter F. Direct measurement of adrenal secretion during operative trauma and convalescence. Surgery. 1962 Jul;52:174-187. •Kehlet H. A rational approach to dosage and preparation of parenteral glucocorticoid substitution therapy during surgical procedures. A short review. Acta Anaesthesiol Scand. 1975;19(4):260-26 •Kehlet H. Clinical course and hypothalamic-pituitary-adrenocortical function in glucocorticoid-treated surgical patients. Copenhagen: FADL; 1976. •Somasundaram Elangovan,A RETHINK ON THE USE OF TOPICAL STEROIDSe-Journal of Dentistry July - Sep 2011 Vol 1 Issue 3 67 references
    68. 68. 68 •Steroid cover for dental patients on long-term steroid medication: proposed clinical guidelines based upon a critical review of the literatureN. Gibson1 and J. W. Ferguson2.British Dental Journal 2004; 197: 681–685  Oral submucous fibrosis: etiology, pathogenesis, and future researchR. Rajendran1. Bulletin of the World Health Organization, 1994, 72 (6): 985-996 •Crispian Scully and Roderick A. Cowson,5TH edition-medical problems in dentistry Chapter-7,endocrine disorder II,p-85-92. •Salem M, Tainsh RE Jr, Bromberg J, et al. Perioperative glucocorticoid coverage. A reassessment 42 years after emergence of a problem. Ann Surg. 1994 Apr;219(4):416-425.
    69. 69. THANKYOU 69
    70. 70. Glucocorticoids antagonists  Mitotane:structure similar to DDT, used in inoperable adrenal cancer  Metyrapone: inhibit 11 -hydroxylase  Aminoglutethamide: inhibit conversion of cholesterol to pregnolone, medical adrenelectomy  Trilostane: inhibit conversion of pregnolone to progesterone; used in Cushing’s syndrome  Ketoconazole: anti-fungal, inhibit CYP450 enzymes, inhibit steroid synthesis in ad.cortex and testis; used in Cushing’s syndrome & Ca.prostate  Mifepristone: glucocorticoid receptor antagonist; anti- progesterone, used in Cushing’s syndrome 70
    71. 71. 71
    72. 72.  The effect of anabolic steroids on muscle mass is caused in at least two ways:first, they increase the production of proteins; second, they reduce recovery time by blocking the effects of stress hormone cortisol on muscle tissue, so that catabolism of muscle is greatly reduced. It has been hypothesized that this reduction in muscle breakdown may occur through anabolic steroids inhibiting the action of other steroid hormones called glucocorticoids that promote the breakdown of muscles.[26] Anabolic steroids also affect the number of cells that develop into fat-storage cells, by favouring cellular differentiation into muscle cells instead. Anabolic steroids can also decrease fat by increasing basal metabolic rate(BMR), since an increase in muscle mass increases BMR 72 Major effects of steroid abuse can include liver damage; jaundice; fluid retention; high blood pressure; increases in "bad" cholesterol. Also, males risk shrinking of the testicles, baldness, breast development, and infertility. Females risk growth of facial hair, menstrual changes, male-pattern baldness, and deepened voice. Teens risk permanently stunted height, accelerated puberty changes, and severe acne. All users, but particularly those who inject the drug, risk infectious diseases such as HIV/AIDS and hepatitis. Most anabolic steroids are synthetic substances similar to the male sex hormone testosterone
    73. 73. 73 This short review should underscore the primary problems associated with the development of ‘guidelines’ defining the appropriate use of intra-articular corticosteroid injection: there is just too little science evaluating short and long term efficacy, assessing the most efficient technique for drug delivery and the most effective formulation, and documenting the risks associated with repeated articular injection. Nonetheless, it is clear that intra-articular injection of the TMJ with local anesthetic and corticosteroid may be useful with some forms of temporomandibular joint disease including juvenile rheumatoid arthritis and uncomplicated TM joint arthralgia associated with acute inflammation and osteoarthritis. However, as is noted by JJ Buescher in the American Family Physician (http://www.aafp.org/afp/2007/1115/p1477.html), “repeated intra- articular corticosteroid injections are not recommended”
    74. 74. 74

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