SHOCK

Definition: Shock is a condition in which circulation fails to meet the nutritional needs of the cells and at the same time fails to remove the metabolic waste products. Or Shock may be defined as an acute, generalized inadequate perfusion of critical organs that, if continued will produce serious pathophysiologic consequences. Stages of Shock: Divided into 3 stages ! a" #arly, $compensated shock$. b" %rogressive, $decompensated shock$. c" &rreversible shock. Early or Compensated Shock: &s due to minor deficiency in the circulating blood volume such as compensatory mechanisms. #g. 'onstriction of the arteriolar bed. (ugmentation of heart rate. &ncrease secretion of (D) *(denosinedihydrogenase".

The Progressive, Decompensated Shock : +his stage of shock appears with persistence of shock, especially when an additional stress is imposed on an individual in $compensated shock$. &n this stage there is ! &ntense arteriolar constriction. &ncrease heart rate. ,

Decline in -% and cardiac output. +echypnea is common *)urried or .aboured -reathing"

!rreversi"le Shock: +his is marked by ! %rogressive reduction in the cardiac output. %rogressive fall in -.%. /orsening of metabolic acidosis. +he reduced blood flow to the brain, heart and kidneys leads to ischemic cell death in these organs with progressive deepening, coma, progressive renal failure and uremia *&ncrease blood urea".

Classification of Shock: ," )ypovolaemic shock or )aematogenic shock. 0" 'ardiogenic shock. 3" +raumatic shock 1" 2eurogenic shock 3" %yschogenic shock 4" Septic shock 5" 6iscellaneous types (naphylactic shock. &nsulin shock.

#$ Hypovolaemic Shock or Haematogenic Shock : 6ost common type seen in patients with ma7illofacial trauma. +his is due to reduction in the amount of fluid pumped through the vascular bed. #7ample,

blood loss, plasma or body water, electrolytes, vomiting, diarrhea and dehydration. +his is clinically manifested by ! .ow cardiac output. +achycardia *increase pulse rate 859" .ow blood pressure : ;asoconstriction.

Clinical Features: Depends on the degree of loss of blood volume and on the duration of shock. Depending on this it is classified as a" 6ild b" 6oderate c" Severe shock 6ild Shock .oss of less than 09< of the blood volume. Clinical Features: 'onstriction of -.;. in the skin. 'ollapse of subcutaneous veins in e7tremities, particularly the feet become pale and cool. Sweating in forehead, hands and feet due to adrenergic discharge. +he patient feels thirsty and cold. 6oderate Shock .oss of blood volume from 09!19<.

Clinical Features : (long with the above findings there will be! Oliguria *decrease urine output". %ulse rate is increase but less than ,99 per minute. .oss of blood volume more than 19< usually leads to severe

Severe Shock shock.

Clinical Features: +here is pallor *skin or e7tremities become pale" .ow urinary output =apid pulse .ow -.%.

+reatment ," =esuscitation +his should be started immediately as the patient is admitted

with hypovolumic shock. +his starts with ! #stablishment of clear air way. 6aintaining adequate ventilation. O7ygenation. %atient should be in ,3 trendlenberg position. 'are should be taken when lowering the head to support the >aws to prevent airway obstruction, and this will improve venous return preventing stasis of blood in the muscles and legs preventing oedema. 0" &mmediate control of -leeding +his is very important in case of haemorrhagic shock. 3" #7tracellular fluid replacement ?luid replacement should be started

immediately after the control of bleeding. 1" Drugs a" Sedatives 'ommonly used to alleviate pain. #g. 6orphine should be given &.;. or S.'. &t is contraindicated in @ 'hildren %atient with head in>ury.

?or children -arbiturates are preferred. 1

6orphine dose &n> morphine ,99 mg&m. 6orphine produces relief of pain and does not alter the other functions of '2S like slurred speech or motor in co! ordination. b" 'hronotropic agents &n patients with decrease heart rate chronotropic agents are used which primarily increase heart rate. #g. (tropine is most widely used in this group. Dose &n> (tropine sulphate 9.43mg is diluted in 3ml of distilled water and

this solution is given slowly through &; route followed by another 9.3ml if radial pulse is not clearly palpable. c" ;asoconstrictions +he main role of this drug is that it @ &ncrease -.%. &ncrease perfusion pressure for coronary circulation.

+he most commonly used drugs are ! %henylephrine 6etaraminol

d" -eta!-lockers +his drug increases efficiency of ventricular contraction. #g. %ropranolal is most widely used drug in this group.

%$ Tra&matic Shock: +his type of shock is caused by ma>or in>uries like @ ?ractures 'rush in>uries -urns #7tensive soft tissue in>uries. &n this type of shock there is hypovolaemia due to bleeding both e7ternally such as lacerations or from internal sources. A&+ bleeding *eg. ulcer". 3

?emoral fractures. 'rush in>uries. =uptured internal organs *eg. liver and spleen".

Clinical Features: Similar to hypovolemic shock. +he differentiating features from hypovoleamic shock are ! a" %resence of peripheral and pulmonary oedema. &nfusion of large volumes of fluid which may be adequate for pure hypovolaemic shock and is usually inadequate for traumatic shock. +reatment ,. =esuscitation needful. 0. .ocal treatment of trauma. 3. 'ontrol of bleeding and surgical debridement of ischemic and dead tissues. 1. &mmobilisation of fractures may be required. 3. ?luid replacement. &n this type of shock mechanical ventilators support is more

Cardiogenic Shock: =esults from intrinsic in>ury to the heart. 6ost common cause @ left ventricular failure secondary to 6yocardial infarction, cardiac arrhythmias or cardiac failure. Clinical Features: &n the early stages the skin is pale and cool. Brine output is low. =apid pulse. (rterial blood pressure becomes low.

&n case of ..;.? the patient has ! Decrease cardiac output. 4

&ncreased pulmonary artery occlusion pressure and pulmonary oedema. &ncreased systemic vascular resistance. %atient has bronchial rales. 3rd heart sound is heard.

&n case of =.;.? the ! 2eck veins becomes distended. .iver may also be enlarged. %eripheral oedema.

+reatment (irway must be clear. (dequate o7ygenation. &f patient complains of pain! &t should be treated with adequate sedative %ulmonary oedema should be treated with a diuretic.

'ardiogenic shock may also be due to ! 'ardiac dysarhythmias. 6itral regurgitation (cute aortic regurgitation or stenosis. (cute viral myocarditis.

'e&rogenic Shock: +his is caused by @ %araplegia Cuadriplegia +rauma to the spinal cord Spinal anaesthesia. 5

+his is due to blockage of sympathetic nervous system resulting in loss of arterial and venous tone with pooling of blood in the dilated peripheral venous system. Clinical Features: +he peculiar feature is that ! +he skin remains warm, pink and well perfused in contradistinction to hypovolaemic shock. Brine output may be normal. )eart rate is rapid. -.%. is low.

;asovagol or ;asogenic Shock &s a part of neurogenic shock in which there is pooling of blood due to dilatation of peripheral vascular system. 'aused due to Decrease venous return to the heart leading to low cardiac output and bradycardia.

Pyschogenic Shock: 'aused by sudden fright from une7pected bad news. Sight of accident etc. &ts effect may vary in intensity from unconsciousness to sudden death. Treatment of 'e&rogenic Shock: ," #levation of legs is effective in treating patients with neurogenic shock. +rendelenburg position *i.e, head end of the bed is lowered". +his position displaces blood from the systemic venules and small veins and thus increases cardiac output.

0" (dministering of fluids increase cardiac output. 3" ;asoconstrictor drug

+his increases filling of the right heart which in turn

-ecause its action is to restore venous tone and thus

restoring cardiac output. &ts prompt action saves the patient from sudden fall in -.%. and decrease cardiac output and from damage to brain, heart and kidneys.

Septic Shock: +his type of shock is most often due to @ Aram negative septicaemia. +his may occur in cases of &"Severe septicaemia, ii"%eritonitis, iii"6eningitis. Aram negative organisms 'oli : -acteroids. Aram positive organisms which cause these types of shock are

&"Stephylococcus, ii"Streptococcus and iii"%neumococcus. Clinical Features: &nitially there is development of chills and cold and increase temperature above ,99?. &ncrease cardiac output. &n late cases vascular permeability increase. decreases leading to hypovolaemia. &n advanced cases cardiac function is damaged due to to7ins liberated by organisms. Treatment: Divided into 0 groups ! a" +reatment of infection by early surgical debridement or drainage and use of antibiotics. b" +reatment of Shock @ includes fluid replacement, steroid administration, use of vasoactive drugs. E So that the blood volume

(ntibiotics Depending on culture and sensitivity test. c" ?luid replacement is very important. +his will provide sufficient blood volume to the vital organs. (iscellaneo&s Types : &nclude @ a" (naphylactic shock. b" &nsulin shock. (naphylactic shock 'ommonly seen after penicillin administration Such

type of shock is said to be due to increase release of histamine and slow release substance *S=S" of anaphyla7is by combination of antigen with ,g# on the mast cells and basophils. )naphylactic Shock: (naphyla7is +his is the classical immediate hypersensitivity reaction. +he term anaphyla7is *ana!without, phyla7is!protection" was coined by =ichet ,E90. Clinical Features : +he clinical features of anaphyla7is are the some with any antigen, but are different in different species. +he clinical features are due to smooth muscle contraction and increased vascular permeability. +he organs affected vary with the species. +he tissues or organs predominantly involved in anaphyla7is reaction are known as $target tissues$ or Fshock organs$. +he other changes seen in anaphyla7is are oedema, decreased coagulability of blood, fall in blood pressure and temperature, leucopenia and

thrombocytopenia. Signs and Symptoms of Anaphylactic shock: -egin with itching of the scalp of tongue. +here may be nausea, vomiting, abdominal pain and diarrhoea, sometimes with blood in the stool, acute hypotension, loss of consciousness and death follow. ,9

(naphyla7is commonly associated with heterogeneous serum therapy is now seen mostly following antibiotic in>ections. &nsect stings can also cause anaphyla7is in man. %rompt treatment with adrenaline can be lifesaving. (drenaline is to be administered, 9.3ml of a , in ,999 solution, sub!cuteneously or intramuscularly, the dose being replaced upto a total of 0.9ml over ,3 minutes if necessary. Cutaneous Anaphylaxis : /hen a small shocking dose of an antigen is administered intradermally to a sensitized host, there will be a local Fwheal and flareF response *local anaphyla7is". +he wheal is a pale, central area of puffiness due to oedema, which is surrounded by a flare caused by hyperaemia and subsequent erythema. 'utaneous anaphyla7is *skin test for type & hypersensitivity" is useful in testing for hypersensitivity and in identifying the allergen responsible in atropic diseases. &n highly sensitized individuals even the skin test may lead to serious and even fatal reactions. )ence, a syringe loaded with adrelalin should always be kept ready whenever a skin test is performed to detect anaphylactic hypersensitivity. Passive cutaneous anaphylaxis (PCA) : +his test developed by Ovary *,E30" is an e7tremely sensitive in!vivo method for detection of antibodies. ( small

volume of the antibody is in>ected intradermally into a normal animal. &f the antigen, along with a dye such as evans blue, is in>ected intravenously 1!01 hours afterwards, there will be an immediate blueing at the site of intradermal in>ection due to vasodilation and increased capillary permeability *wheal and flare reaction". %'( can be used to detect human &gA antibody which is

FheterocytotropicF *capable of fi7ing to cells, of other species", but not &g# which is FhomocytotropicF *capable of fi7ing to cells of homologous species only".

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Anaphlaxis in-vitro : &solated tissues, such as intestinal or uterine muscle strips from sensitized guinea pigs, held in a bath of rings solution will contract vigorously on addition of the specific antigens to the bath. +his is known as Schultz!Dale %henomenon. +he reaction is specific and will be elicited only by the antigen to which the animal is sensitive. echanism of Anaphylaxis : (naphylactic hypersensitivity can be passively transferred from a sensitive donar to a normal recipient by in>ection of serum. +his passive sensitization establishes that the reaction is determined by circulating antibody. )omocytotropic &g# antibody is the ma>or antibody responsible for anaphylactic hypersensitivity. +o a lesser e7tent heterocytotropic &gA may be responsible. &gA molecules are bound to surface receptors on mast cells in tissues and basophils in circulation. ?ollowing e7posure to the shocking dose, the antigen molecules combine with the cell bound &g#, bridging the gap between ad>acent antibody molecules. +his cross linking increases the permeability of the cells to calcium ions and leads to degranulation with release of biologically active substances contained in the granules. +he manifestations of anaphyla7is are due to pharmacological mediators, which are of 0 kinds ! +he primary mediators which are the preformed contents of mast cells and basophil granules, *histamine, serotonin, easinophil chemotactic factor of anaphyla7is, neutrophil chematoctic factor, heparin and various proteolytic enzymes". +he secondary mediators which are newly formed upon stimulation by mast cells, basophils and other leukocytes *slow reacting substance of anaphyla7is, prostaglandins and platelet activating factors".

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!$ Primary (ediators of )naphyla*is: !istamine : +his is the most important vasoactive amine in human anaphyla7is. )istamine is formed by the decarbo7ylation of histidine found in the granules of mast cells, basophils and in platelets. =eleased into the skin, histamine stimulates sensory nerves, producing burning and itching sensations. &t causes vasodilation and hyperaemia by an a7on refle7 *flare effect" and edema by increasing capillary permeability *wheal effect". )istamine induces smooth muscle contraction in diverse tissues and organs, including vasculature, intestines, uterus and especially the bronchioles. &t also stimulates secreations *secretogogue effect". Serotonin ("-hydroxy tryptamine) : +his is a base derived by decarbo7ylation of tryptophas. &t is found in the intestinal mucosa, brain tissues and platelets. &t causes smooth muscle contraction, increased capillary permeability and vasoconstruction. &t is important in anaphyla7is in rats and mice, but its role in man is uncertain. Chemotactic factors : +he eosinophil chemotactic factors of anaphyla7is *#'?!(" are acidic tetrapeptides released from mast cell granules which are strongly chemotactic for eosinophils. +hese probably contribute to the eosinophilic ( high molecular weight

accompanying many hypersensitivity states.

chemotactic factor has been identified, which attracts neutrophils. )eparin is an acidic mucopolysaccharide. &t contributes to anaphyla7is in dogs, but apparently not in man. !!+ Secondary (ediators of )naphyla*is : #) Slo$ reacting su%stance of anaphylaxis (S&S-A) : +his is so called because of the slow but stained contraction of the smooth muscles that it causes. produced by leukocytes, mainly in lungs. ,3 &t is

+hey act on the smooth muscles of the larger blood vessels and of the bronchi and may be responsible for the prolonged respiration distress in asthma. +hey are much more potent bronchoconstrictors than histamine and are not inhibited by antihistaminics. Prostaglandins and 'eukotrienes : +hey are derived by two different pathways from arachidonic acid, which is formed from disrupted cell membranes of mast cells and other leukocytes. +he lipo7ygenase pathway leads to the formation of leukotrienes, while the cyclo!o7ygenase pathway leads to prostaglandins and thrombo7ane. %rostaglandin ?0a and thrombo7one (0 are powerful, but transient, bronchoconstrictors. %rostaglandin #0 is a bronchodilator. %rosthaglandins also effect secreation of mucous glands, platelet adhesion, permeability and dilation of capillaries and the pain threshold. Platelet activating factors (PAF) : &s a low molecular weight lipid release from basophils during immediate hypersensitivity. &f causes aggregation of platelets and release of their vasoactive amines. Other (ediators of )naphyla*is: =esides the products of mast cells and other leukocytes, several other biologically active substances have been implicated in anaphyla7is. +hese include the anaphylato7ins released by complement activation and bradykinin and other kinins formed from plasma kininogens. Anaphylactoid reaction : &ntravenous in>ection of pentone, trypsin and certain other substances provokes a clinical reaction resembling anaphylactic shock. +his is termed Fanaphylactoid reactionF. +he clinical resemblance participating in both the reactions. +he only immunological basis and is a non!specific mechanism involving the activation of complement and the release of anaphylato7ins. (anagement of Shock in Dental Clinic: ,1

Shock can be more easily prevented than treated. &n prosthodontics at times neurogenic, anaphylactic and septicaemic shock may be seen. +reatment should be aimed at determination of the cause for shock for better management. &t can be caused due to ! (n7iety Drugs *local anesthesia" Surgery *placement of implants".

,eneral Principles in (anagement of Shock: ,. -est treatment of shock is prevention. &f shock cannot be prevented one should concentrate on limiting its depth and duration. 0. Detect the underlying cause of shock, eg. &f shock is due to volume loss, the cause of volume loss must be stopped and immediate volume replacement instituted. &f problem is due to sepsis underlying site of infection, causative organism should be isolated and treated with appropriate antibiotics. 3. +he patient condition and severity of shock should be measured at regular intervals. 1. ?requent monitoring especially of ventilation, acid!base balance, fluids and electrolytes should be done. ( clinical state which is most commonly seen in a dental clinic which may be seen in the form of shock is syncope. Syncope &s defined as a sudden, transient loss of consciousness, usually

secondary to cerebral ischemia. %redisposing ?actors ?actors that can precipitate syncope may be divided into 0 groups %hychogenic factors ! ?right 2on!phychogenic factors ! )unger ,3

! (n7iety ! #motional stress ! Bnwelcome news ! %ain G sudden, une7pected. ! Sight of surgery and other dental instruments.

! #7haustion ! %oor physical condition ! )ot, humid, crowded environment

'linical 6anifestations 6ay be grouped into three phases. %resyncope. Syncope %ostsyncope *recovery period".

#arly ?eeling of warmth in neck and face. .oss of color, pale or ashen!gray skin tone. )eavy perspiration 'omplains of feeling faint 2ausea -.%. appro7imately baseline =apid heart rate *eg. ,09 per minute".

.ate %upillary dilation Hawning )yperpnea 'oldness in hands and feet )ypotension -radycardia Dizziness ,4

;ascular disturbances .oss of consciousness

(anagement of Syncope: Step , %lace patient in supine position with feet slightly elevated. Step 0 ! #stablish patient airway. ! )ead tilt chin lift method ! 'heck breathing ! Iaw thrust maneuver if necessary. ! 'heck circulation. Step 3 ! 6onitor vital signs ! -.%. ! )eart rate ! =espiratory rate. Support %atient ! (mmonia vaporole crushed under nose of patient. ! -lankets if cold or shivering ! =eassure patient. Step 1 6aintain your composure Step 3 ?ollow!up treatment. ! Determine factors causing unconsciousness. ! %revent recurrence of syncope. ! (rrange for patient to be taken home by friend or relative. ! 2o further dental treatment for 01 hours.

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