Haemorrhage & Shock

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Good Morning1

Haemorrhage&ShockPresented by : Dr. Himanshu JataniaModerated by: Dr. V.K. Joshi Dr. Venkatesh Anehosur2Contents1. Definition2. Classification3. Normal physiology of hemostasis4. Clinical features5. The Surgical patient & Risk of Haemorrhage6. Methods of determining blood loss.7. Haemorrhage control - Mechanical, Thermal & Chemical means8. Local & Systemic Hemostatic Agents9. Fluid Replacement10. Special Clinical Considerations 11. Conclusion12. References

3Definition

the flow of blood from a ruptured blood vessel (normally due to injury)

escape of blood from the circulatory system

- a heavy release of blood within or from the body

The term "haemorrhage" comes from the Greek "haima" blood + rhegnumai" to break forth = a free and forceful escape of blood.

4Classification

Source Arterial, venous or capillary

External Appearance

Internal or concealed

Primary

Time of appearance Reactionary

Secondary

Haemorrhage may be......5Arterial Bright red, spurting as jet with each systole.

Venous Dark red, steady and copious E.g. Varicose veins, oesophageal varices in portal hypertension.

Capillary Bright red, often rapid can be can be serious in haemophilia.

6* Primary haemorrhage - At the time of injury or operation* Reactionary haemorrhageFollows primary haemorrhage within 4 to 6 hours. Causes (1) Slipping of ligature (2) Dislodgement of clot (3) Cessation of reflex vasospasm.Raise in BP, restlessness * Secondary haemorrhageOccurs in 7 to 14 days because of infection and sloughing of vessel wall (usually artery). Predisposing factors are pressure of a draining tube, the presence of a fragment of bone, a ligature in an infected area

7 AcuteOnset Chronic

Mild

Severity Moderate

SevereMild haemorrhage Blood loss is less than 500ml. E.g. minor oral surgical procedure.

Moderate haemorrhage Loss is upto 2L. Initially BP falls but is restored by increased PR.

Severe haemorrhage Could be more than 2L. Due to positive feed back mechanism BP falls significantly hence is lethal.

8Hemostasis

Normal hemostasis is dependent upon the complex interaction of plasma coagulation and fibrinolytic proteins, platelets, and the blood vasculature

Haemostasis consists of 3 phases:

Vascular phasePlatelet phaseCoagulation phase

Primary Hemostasis (Platelet Plug)Secondary Hemostasis (Fibrin)9Vascular Phase

Local control - Vasoconstrictors such as thromboxane are released at the site of the injury.

Systemic control - Epinephrine released by the adrenal glands stimulates general vasoconstriction.

Platelet Phase

The administration of heparin does not interfere with this reaction and that fact explains why haemostasis can occur in the heparinized patient

When a blood vessel is damaged, the blood is exposed to collagen fibers in the basement membrane of the vessel (shown in green below). Platelets stick to collagen and become activated. Activated platelets release chemicals such as ADP, and thromboxane, that cause the aggregation of more platelets to the site of injury. Platelet aggregation results in the formation of a platelet plug which acts to stem the flow of blood from the broken vessel.

VWF :Initial platelet adhesion is to von Willebrand's factor (VWF), previously secreted by endothelial cells into the subendothelium. VWF binds to receptors on the platelet surface membrane10

Clotting Factors11Coagulation Phase

Liquid blood -> semi solid gel

Fibrinmonomers come from an inactive precursor calledfibrinogen. The body of the fibrinogen molecule has caps on its ends that mask fibrin-to-fibrin binding sites. If the caps are removed then fibrin monomers polymerize to form fibrin polymers. This process requiresthrombin, the enzyme that converts fibrinogen to fibrin. This process also requirescalcium, which acts as a kind of glue to hold the fibrin monomers to each other to form the polymeric fiber. The fibrin fibers form a loose meshwork that is stabilized by clottingfactor XIII. The stabilized meshwork of fibrin fibers traps erythrocytes, thus forming a clot that stops the flow of blood.12

Thrombin : How ? Why ?If thrombin is present then clotting will proceed, but if thrombin is absent then clotting will not occur. How then is thrombin controlled? Thrombin is derived from an inactive precursor called prothrombin. There are two pathways that lead to the conversion of prothrombin to thrombin; (1) the intrinsic pathway and (2) the extrinsic pathway.13

14Inhibition of Excessive Clotting

Clotting factors are rapidly inactivated - enzymes in the blood -> inactivate clotting factors.

Fibrin fibers inhibit the activity of thrombin - fibrin fibres have an inhibitory effect on activity of thrombin -> negative feedback loop

Clot Removal

As clotting factors are taken away from the site of injury by the blood stream, they become inactivated by these enzymes. This ensures that clotting will only occur at the site of injury and not progress steadily down the vessel.tissue plasminogen activator(TPA)is an enzyme that catalyzes the conversion ofplasminogentoplasmin. Plasminogen is an inactive precursor molecule found in the blood, but plasmin is an enzyme that dissolves clots. Plasmin levels are not very high so clot removal is a slow process. By the time the clot has been completely dissolved by plasmin, the vessel has had a chance to heal itself. In summary, the clot, which forms rapidly, calls for its own destruction by initiating the activation of plasmin.It is essential that platelets become activated only at the site of a broken vessel. Otherwise activated platelets would form plugs and induce clots in inappropriate places. Healthy vessels secrete an enzyme called prostacyclin that functions to inhibit platelet activation and aggregation.15 Inhibitors Of Hemostasis

Primary Hemostasis : 1) Prostacyclin 2) Nitric oxide

Secondary Hemostasis: 1) Antithrombin (AT) 2) Heparin cofactor II 3) PROTEIN C 4) PROTEIN S 5) Thrombomodulin

16clinical features PallorTachycardia Tachypnoea Rapid thready pulseHypotension OliguriaCold clammy skin due to vasoconstrictionDry face, dry mouth and goose skin appearanceThirst Anxiety, confusion and unconsciousness

17The Surgical patient & Risk of Haemorrhage Major Risk Factors Minor Risk Factors1. Obstetric Bleeding

Liver Disease

3. Renal Disease

4. Known hereditary diseases

History of abnormal blood count

6. MedicationsHistory of unusual bleeding

Frequent episodes of epistaxis

Unusual mucosal bleeding

4. Abuse of illicit drugs-d/t chronic alcohol abuse or Hepatitis-Hemophilia-Leukemia-NSAIDs,Aspirin,Anticoagulants,Antibiotics,Chemotherapeutic agents

18 Low-Risk Patients Moderate-Risk Patients High-Risk PatientsNo history of bleeding from previous surgery

No family H/O coagulopathies

No H/O excessive bleeding

No H/O liver disease

No H/O heavy alcohol usage

Not taking any medication known to cause bleedingH/O abnormal bleeding following tooth extraction or other minor surgery

A family H/O bleeding

Abnormal bruising without trauma

H/O liver disease

Alcoholic

History of malabsorption

Long term antibiotic usagePatient is known to have a coagulopathy

Documented family history of bleeding

Patient taking warfarin or heparin (within 4 hours)19 Risk Category Action Required Low-risk patient Proceed with surgery. No further investigation or laboratory testing is required. Moderate-risk patientA more detailed history should be obtained and the potential risk assessed.Laboratory testing: Bleeding profile, bleeding time, and platelet count. Consult with physician if necessary. Optimize patient preoperative: the treatment to optimize the patient will depend on the results of the findings that contribute to the risk factors. High-risk patientConsult with a hematologist. Laboratory testing: Bleeding profile, bleeding time, and platelet count. Management of bleeding problems before surgery. Postoperative management.20 Blood clot: A clot size of a clenched fist is roughly equal to 500ml.

Swelling in closed fractures: Moderate swelling in closed fracture of the tibia equals 500-1500ml of blood loss.

Moderate swelling in a fractured shaft of femur equals 500-2000ml of blood loss.

Swab weighingBlood loss = Weight of swab after use dry weight of swab.To this add blood collected by suction or in drainage bottle.1gm=1ml

Multiply this value by 1 to compensate for the water lost from the plasma by evaporation ( in major surgeries)21Methods of determining blood loss21Prime task is to stop bleedingLOCAL HAEMOSTASIS- Mechanical- Thermal- Chemical Mechanical

Digital Pressure: Finger -> least traumatic vascular hemostat

Haemostat -> temporary mechanical device to stem bleeding.

Large areas - packs -> hot or cold ??

The oldest mechanical device to effect closure of a bleeding point or to prevent blood from entering the area of disruption is digital pressure.

The obvious disadvantage of digital pressure is that it cannot be used permanently.

Direct pressure applied by means of packs affords the best method of controlling diffuse bleeding from large areas.

Unless the heat is so great as to denature proteins it may actually increase bleeding, whereas cold packs promotes haemostasis by inducing vascular spasm at increasing endothelial adhesiveness.

22 LIGATION

In general, a ligature replaces the haemostat as a permanent method of effecting haemostasis in a single vessel.

When a vessel is transected, a simple ligature usually is sufficient.

For larger arteries with pulsation and longitudinal motion, transfixation suture to prevent slipping is indicated.

The adventitia and media constitute the major holding forces within the walls of large vessels, and therefore multiple fine sutures are preferable to fewer larger sutures .

23Ligation of common carotid artery It is done at level of hyoid bone where very few structures pass across them.

They are middle thyroid vein and artery and internal jugular vein and superficial arteries.

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Ligation of ECAUsually ligated above superior thyroid artery because the superior thyroid artery arises at low level hence no room for ligation.

25Ligation of Lingual Artery The artery is usually ligated beneath the hyoglossus muscle in the second part of its course Ligation of deep lingual artery is by placing an incision on lateral part of floor of mouth where it just lies beneath the mucosa and ligated as it emerges from hyoglossus.

For unilateral operations on tongue - ligate the artery of that side and for tip operations both the arteries have to be ligated.

It is composed of three parts: the first, from its point of origin to the posterioredge of the hyoglossus muscle; the second, the part beneath the hyoglossus muscle; and the third, the part beyond this muscle to the tip of the tongue.

26Ligation of maxillary arteryLigation of maxillary artery is required in many instances in maxillofacial surgeries, e.g. TMJ surgeries, primary haemorrhage during maxillary osteotomies or during maxillectomies.

It is done through transantral approach where we can visualize the first part of artery in the pterygomaxillary fissure and ligateLigation of facial artery As it branches from the ECA and enters into the submandibular triangle above the stylohyoid muscleAs it emerges onto the face along the anterior border of the masseter muscle.

27EmbolizationIt involves the selective occlusion of blood vessels by purposely introducing emboli.

Interventional radiologist and Interventional neuroradiologists. Indicated in haemangiomas, A-V malformations and epistaxis.

Position of the correct artery or vein supplying the pathology in question is located by Digital Substraction Angiography [DSA] Advantages

Minimally invasiveNo scarringMinimal risk of infectionNo or rare use of general anaestheticFaster recovery timeHigh success rate compared to other procedures Disadvantages

User dependent success rateRisk of emboli reaching healthy tissueNot suitable for everyoneRecurrence more likelyA distinct advantage of embolization over surgical ligation is the more selective blockade of smaller branches. By embolizing just the bleeding branch, normal blood flow to the remainder of the vessel is retained. 2829

The procedure was simple: a piece of metal was heated over fire and applied to the wound. This would cause tissues and blood to heat rapidly to extreme temperatures in turn causing coagulation of the blood thus controlling the bleeding, at the cost of extensive tissue damage.ThermalCauters30Heat achieves haemostasis by denaturation of protein, which results in coagulation of large areas of tissues.

In cauterization heat is transmitted from the instrument by conduction directly to the tissues.

Electrocautery has replaced direct heat application.

Electrocautery works by a process of induction from an alternative current source.

When electrocautery is employed an amplitude setting should be high enough to produce prompt coagulation but not so high as to set up an arc between the tissue and cautery tip.The advantage of cautery is that it saves time, and its disadvantages that more tissue is necrosed than in comparision with precise ligature.Direct currents in the range of 20-100mA have been applied to control bleeding from large serous surfaces.

31It represent a new form of electrocautery, more effective than standard electrocautery

In this coagulator, monopolar current is transmitted to tissues through the flow of argon gas.

This allows bleeding from vessels that are smaller than 3mm in diameter to be controlled without the use of haemostats or ligatures.

There is possibility of gas embolism, as there is stream of gas in direct contact with tissues.Argon beam coagulator

32Cryosurgery

At the other end of the thermal spectrum, cooling has been applied to control bleeding.

Direct cooling with iced saline is effective and acts by increasing the local intravascular haematocrit and decreasing blood flow by vasoconstriction.

Temperature ranging between -20C to -180C are used and freezing occurs around the tip of the cannula within 5 sec.

At this temperature, the tissue, capillaries, small arterioles, and venules undergo cryogenic necrosis.This is caused by dehydration and denaturation of lipid molecules.

33In1909, fibrin was used for the first time forhemostaticpurposes byBergel.

In1911,Cushingused fragments of raw muscle and solidified blood clots forhemostasisand noted no adverse effects.

Characteristics of an Ideal hemostatic agent:

capability to stop arterial or venous bleeding within 2 min of application when applied to an actively bleeding wound(2) no requirement for mixing or pre-application preparation(3) simplicity of application (4) light weight and durable (5) long shelf life (6) safe to use with no risk of injury to tissues or transmission of infection(7) Inexpensive.

Chemical a vascular surgeon may want something that polymerizes very quickly in order to stop bleeding, but does not cause clot of the vessel that they spent all this time anastomosing, where as a reconstructive surgeon for example may want something that polymerizes very slowly to give them time to reposition their flaps or grafts.34

35

Gelatin foam (absorbable gelatin sponge)

Commercially known as Surgifoam.

Introduced in 1940s by Dr. Gray.

It is the porous, pliable sponge made from dried and sterilized porcine skin gelatin.

It does absorb approximately 45 times its weight in blood and can expand to approximately 200% of its initial volume.

Absorbed in approximately four to six weeks 36

It is a sterile mixture of bees wax, paraffin and isopropyl palmitate.

It is useful when bleeding is from a visualized local vascular channel within bone, bone bleeder, this occurs commonly during the extraction of mandibular third molars.

The wax is pliable enough to be placed within a vascular channel, immediately tamponading the vascular source.

It is non resorbable and due to its possible adverse effect on osteogenesis caution should be used where regeneration of bone is expected.Bone wax softening agent such as paraffininhibits formation of new boneosteogenesisand acts as a physical barrier preventing bone union.For this reason bone wax is almost never used in areas where bone fusion is criticalBone wax remains as aforeign bodyfor many years, and can cause agiant cellreaction and local inflammation.37Oxidized regenerated cellulose{Surgicel / Oxycel}

It is a resorbable oxidized cellulose material.

After it is fully absorbed with blood, it swells into a brownish or black gelatinous mass that aids in clotting.

Relatively acidic and is thought to cause some small vessel contraction.

Relatively bacteriostatic when compared to other hemostatic agents.

Needs to be applied dry and absorbs within four to eight weeks.

On post-op imaging surgicel sometimes causes a ring-enhancing lesion which can be mistaken for an abscess cavity or tumor recurrence.

because of its relatively low pH, it deactivates and denatures some of the bacterial proteins especially those related to antibiotic resistance, thus making them more susceptible to antibiotics38Microfibrillar collagen (MFC)Commercially known as Avitene

This is collagen, which is derived from bovine skin.

Binds tightly to blood surfaces, so a relatively dry field is not necessary for application.

Works slightly different because in addition to being collagen and causing contact activation, it does somehow directly activate platelets.

It is absorbed in three months. 39

Hemostatic Gauze 40

A styptic or hemostatic pencil is a short stick ofmedication, usuallyanhydrous aluminium sulfate,potassium alum (both are types ofalum) ortitanium dioxidewhich is used for stanchingbloodby causingblood vesselsto contract at the site of the wound.Anastringent substance is a chemical compound that tends to shrink or constrictbody tissues, usually locally aftertopical medicinal application.

Agents- Tannins [wines & tea] Alum Oatmeal Banana skins Calamine lotion

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Fibrin GlueFibrin glueis a synthetic substance used to create afibrinclot.It is made up offibrinogenandthrombinthat areinjectedthrough one head into the site of a fibrin tear. Thrombin acts as anenzyme and converts the fibrinogen into fibrin between 10 and 60 seconds and acts as atissue adhesive.42

Adrenaline Adrenaline is added in concentration of 1:80,000 in xylocaine.

It is used for hemostatic purposes because it; - causes vasoconstriction - reduces capillary haemorrhage

Side effect of adrenaline is, it produces undesirable cardiac arrhythmias.

Also has the disadvantage of producing local tissue cyanosis and acidity.

The use of adrenaline as a local hemostatic agent is controversial as it may cause rebound vasodilatation.43Newer Products1. CHITOSANChitosan hemostats are topical agents composed of chitosan and its salts.

Chitosan bonds with platelets and red blood cells to form a gel like clot which seals a bleeding vessel.

Unlike other hemostat technologies its action does not require the normal hemostatic pathway and therefore continues to function even when anticoagulants like heparin are present.

Chitosan is used in some emergency hemostats which are designed to stop traumatic life threatening bleeding.

2. ZEOLITE

3. FIBRIN BASED DRESSING (American Red Cross Dressing)44 Systemic agents

Adrenochrome monosemicarbazone - obtained by theoxidationofadrenaline.Reduces capillary fragility Controls oozing from raw surfacesPrevents microvascular bleeding

Ethamsylate - 250-500 mg 4-6 hrly as needed increasescapillaryendothelialresistance promotesplateletadhesion

AntifibrinolyticsTranexamic acid - 1-1.5 g 2-4 times/day competitively inhibits breakdown of fibrin clots. It blocks binding of plasminogen and plasmin to fibrin, thereby preventing haemostatic plug dissolution.

45Botropase(Aqueous solution of HAEMOCOAGULOSE isolated from VENOM OF BOTHROPS JARARACA , containing 0.9% of NaCl)MOA - Botropase acts on fibrinogen to produce a fibrin monomer that can be converted by thrombin to a fibrin clot. The action of Botropase in this way is similar to that of thrombin.

The action of thrombin may be inhibited by the antithrombin normally existing in the blood, whereas the action of Botropase continues, even when antithrombin is present. By the action of either thrombin or Botropase, the terminal amino acids in the fibrin clots consist of tyrosine and glycine; however, the ratio is of 1:2, in the former and in the latter it is 1:1. Unlike thrombin, Botropase is not absorbed by the fibrin clots and is therefore not neutralised by that mechanism, as occurs with thrombin.

ADULTS :- 1ML I.M. SOS UPTO 2-3 TIMES A DAY. CHILDREN :- 0.5 -0.7 ML ACCORDING TO THE AGE AND SERIOUSNESS OF HAEMORRHAGE.46Fluid replacement Crystalloids Isotonic crystalloids - Ringers lactate - 0.9% NaCl

Hypertonic saline solutions - 3% NaCl - 7% NaCl

Hypotonic solution - 0.45% NaCl

Colloids - Human plasma - Albumin: 5%, 25% - Dextran Expands plasma volume up to 24 hours - Degraded gelatin ( 3.5% ) Haemaccel - Poly vinyl pyrrolidine ( 3.5% )

47Blood & Blood Substitutes IndicationsTrauma with severe blood loss. E.g. long bone fractures, liver & spleen lacerationsMajor operative procedures in which a certain amount of blood loss is inevitable. E.g. head and neck cancer surgeriesFollowing severe burns in which, there is associated haemolysis.Preoperatively in cases of chronic anemia in which surgery is indicated urgently . To arrest haemorrhage, or as a prophylactic measure prior to surgery; in a patient with a haemorrhagic state such as thrombocytopenia, haemophilia or liver disease Fresh whole bloodThis term refers to blood i.e. administered within 24 hr of its donation.

Packed red cells Packed red cells is the product of choice for most clinical situations.Essentially it provides oxygen carrying capacity.

OthersFresh Frozen Plasma, Cryoprecipitate, Platelets, Autologous Transfusion.

48Haemorrhage In Oral & Maxillofacial SurgeryBleeding from a tooth socket

Most common post op haemorrhage encountered by the dental surgeon.

Most common cause of persistent primary haemorrhage is preexisting local inflammation at the site of wound.

Small puncture wounds in the sulcus opposite an upper canine or a lower second molar due to a slip with an instrument can damage the upper labial artery or the facial artery and can be cause of profuse, persistent haemorrhage which may be thought mistakenly to be coming from the socket.

Secondary haemorrhage is fortunately a rare complication of tooth extraction.49Treatment Soft Tissue Hard Tissue

Pressure packs Hemostatic AgentsSuturing Stay sutures e.g. Figure of 8Hemostatic Agents ElectrocauteryLigation of main vessel50Haemorrhage in orbitSome degree of retrobulbar haemorrhage is common in orbital trauma and is recognizable on CT imaging as patchy areas of increased attenuation. Cadaver experiments in the young show that the orbital septum can withstand pressures between 70-100mm Hg before rupture.

In the elderly the septum is weaker and as little as 10-15mm Hg pressure may be enough to cause rupture.

Nose blowing can cause intranasal pressure as high as 114mm Hg and if there is a wall defect in the orbit, air can be transmitted into the orbit.

Unfortunately retinal vessels and the optic nerve cannot withstand pressures of 65-70mm Hg for long and blindness may ensue.

51Signs of Retrobulbar Haemorrhage

tense or expanding proptosisophthalmoplegia increased intraocular pressure loss of pupillary reflexes optic disc or retinal pallor.

TreatmentMannitol 20%, 2gm / kg IV over 5 min.Megadose steroid therapyAcetazolamide 500mg I.V. and then 1000mg orally over 24 hrs.Surgical decompression remains the most certain option - lateral canthotomy with cantholysisIf visual acuity is deteriorating a four wall decompression under LA is required to prevent a permanent loss of vision.52Haemorrhage in cancer patientsCarotid artery blowout

Etiology: carotid artery blowout may occur after a radical neck dissection.

Slough or skin flaps Pre-op and /or post-op radiotherapy.FistulaInfection 53Prevention

Administer pre op, intra op and post op antibiotics.

Cover arteries with viable muscle (E.g. levator scapulae muscle flap) or PMM.

Do not use preoperative radiotherapy.

Allow no dead space over vessels (e.g. in the supraclavicular area or in the submandibular area), especially near the angle of the jaw.

Close all intraoral defects in a water tight manner.

Do not perform vascular reconstruction in the presence of infection 54 Haemorrhage after rhinoplasty

The incidence of excessive bleeding following septorhinoplasty is approximately 2% - 4%.

But can be as high as 10% when simultaneous turbinate surgery is performed.

The anterior ethmoid and sphenopalatine vessels are usually involved.

One of the prime concern with intranasal bleeding is that an unrecognized and untreated septal haematoma can lead to saddle nose deformity.55Epistaxis(or anosebleed) is the relatively common occurrence ofhaemorrhage from thenose.Initial management of epistaxis includes compression of the nostrils and plugging of the affected nostril with gauze or cotton that has been soaked in a topical decongestant. ManagementComplications of nasal packing procedures include septal hematomas and abscesses, sinusitis, and pressure necrosis .

Local - Chronic sinusitis, Epistaxis digitorum (nose picking), Foreign bodies, Intranasal neoplasm or polyps, Irritants (e.g., cigarette smoke), Medications (e.g., topical corticosteroids), Rhinitis, Septal deviation, Septal perforation, Trauma, Vascular malformation or telangiectasia

Chronic-Hemophilia, Hypertension, Leukemia, Liver disease (e.g., cirrhosis), Medications (e.g., aspirin, anticoagulants, nonsteroidal anti-inflammatory drugs), Platelet dysfunction, Thrombocytopenia

56

57

Anterior nasal pack 58

59

Posterior nasal pack Progerssive management may involve direct intranasal cauterization, anterior nasal packing or nasal balloon tamponade.

Persistent bleeding, in some cases, may require transantral ligation of the sphenopalatine artery, ligation of the anterior or posterior ethmoidal artery or possible angiography and embolization.

Antibiotics that coverStaphylococcusspecies (eg, cephalexin, amoxicillin, ampicillin) can preventsinusitis andtoxic shock syndrome.Admit all patients with posterior packing to the hospital for observation.Reflex bradydysrhythmia can develop because of stimulation of the deep posterior oropharynx by the packing.Airway compromise may develop.

60The vessels at risk during TMJ surgery are the superficial temporal artery and vein, the maxillary artery, and the middle meningeal artery.

If the vessels are encountered, ligation may be necessary to ensure haemostasis.

At the level of the lateral capsule, a vein is usually encountered, which also must be cauterized or ligated to ensure haemostasis.Haemorrhage during TMJ surgery61Site Type Management

Primary HaemorrhageTemporalis muscle Venous Dry gauze (Raytec gauze)

Squamous temporal bone Venous Horselys bone wax and/or diathermy

Periarticular Venous Oversew the bleeding points

Maxillary/ Mandibular Arterial Firm packing - repositioning of retractorsartery Check whether pt. is hypertensive Secure bleeder with hemostat followed by Weck arterial clip

Pterygoid plexus Venous Oxycel & dry gauze. If unsuccessful, a bismuth iodoform paraffin gauze is placed

Secondary Haemorrhage Resuscitate & explore wound. Triple antibiotic therapy. 62 Maxillary

Pterygoid plexus, Greater palatine vessel, Nasopalatine vessels and maxillary artery. Mandibular

Maxillary artery, Facial artery, Inferior alveolar vessels Retromolar vessels and pterygoid plexus.Haemorrhage during Orthognathic surgerySource of bleeding63Careful cutting of lateral wall of antrum & avoid resecting descending palatine artery.

Osteotomy cut should be as low as possible.

Maxillary artery is at risk during disjunction of pterygoid, large curved osteotome may cause damage to maxillary artery hence swan neck osteotome must be used.

Prevention64ConclusionA surgeon, in his daily practice, comes across numerous patients presenting with haemorrhage due to a variety of causes and should be adept in measures to be used in the management of such cases.

Apart from achieving hemostasis, one should carefully monitor the patient to assess the quantity of blood loss and should perform adequate replacement therapy in the form of administration of blood, blood products or substitutes, as indicated in individual cases.

Also, one should be aware of the potential complications of such therapy upon the occurrence of which ideal treatment should be instituted.65References

Bailey and Loves - Short Practice of Surgery

Schwartz Shires Spencer - Principles of Surgery

Concise text book of surgery - S. Das

Sreenivasan B. - Textbook of Oral and Maxillofacial Surgery

Essentials of Pharmacology - K.D. Tripathi

Rowe & Williams - Maxillofacial Injuries Vol. I

The Internet

66Next Week....

Shock67

Good Morning68 Haemorrhage in Maxillofacial Trauma

AIRWAY

Lookistenfeebecause airway compromise can occur rapidly and insidiouslyPatency, Level of consciousness, Maxillofacial injury, Stridor or cyanosis

69Blood clot, saliva, bone, teeth or parts of denturesBackward displacement of the tongue.Downward and backward displacement of a fractured maxilla Maxillofacial injuries that compromise the airway70 Haemorrhage in Maxillofacial TraumaBREATHINGStridor - upper airway obstructionGurgling - presence of clotWheezing - lower airway obstruction

All patients who have sustained major trauma above levels of clavicles must be assumed to have sustained a C-spine injury until proven otherwiseRateChest wall movementTracheal deviation Airway foreign bodies, aspiration, inhalation injury pneumothorax Haemothorax71 Haemorrhage in Maxillofacial TraumaCIRCULATIONASSESSMENT:Heart rateSystolic BP and Pulse pressurePeripheral pulsesSkin condition/perfusion/Capillary refillSensoriumHaemorrhage 72

Maxillofacial bleedingDirect pressure.Avoid blind clamping in wounds.

Nasal bleeding:Direct pressure.Anterior and posterior packing.

Pharyngeal bleeding:Packing of the pharynx around ET tube. Bleeding from facial injuries typically is profuse but rarely causes hypovolemia or shock. In hypotensive patients, look for other sources of blood loss such as intrathoracic, intraabdominal, and retroperitoneal hemorrhage. We must try to control bleeding with direct pressure. Blind clamping should be avoided because injury to important nonvascular structures such as the facial nerve and parotid duct can result. Anterior and posterior packing may be needed in patients with nasal bleeding that does not resolve with direct pressure alone. Pharyngeal bleeding may require packing around the ET tube. 73

2 transnasal Foley catheters, placed under traction to provide maxillofacial compression.intubated, with 2 transnasal Foley catheters and a pulse oxymeter on his upper lip.74

Despite recognition of a post traumatic syndrome by Greek physicians such as Hippocrates and Galen, the origin of the term shock is generally credited to the French surgeon Henri Francois Le Dran, who in 1737 defined the same in A treatise of reflections drawn from experience with gunshot wounds and coined the term choc to indicate a severe impact or jolt. An inappropriate translation by the English physician Clare, in 1743, led to the introduction of the word shock to the English language to indicate the sudden deterioration of a patients condition when major trauma has occurred.

It was Edwin A. Moses, who began to popularize the term, using it in his article A practical treatise on shock after operations and injuries in 1867.

75a rude unhinging of the machinery of life

the collapse and progressive failure of the cardiovascular system

Shock is defined as the presence of inadequate organ perfusion and tissue hypoxia resulting in end organ damage. [ Fonseca, 2nd Ed. Vol. II ]

Shock is the clinical syndrome that results from inadequate tissue perfusion [ Harrisons Internal Medicine, 17th Ed. Vol. II ]

Simply stated, shock results from inadequate perfusion of the bodys cells with oxygenated blood.

History states, shock was defined as

a more recent definition calls shock

With insufficient delivery of oxygen and glucose , cells switch from aerobic to anaerobic metabolism. If perfusion is not restored in a timely fashion , cell death occurs.

76CLASSIFICATION OF SHOCK ACCORDING TO HINSHAW AND COX [1972]Hypovolemic shockCardiogenic shockDistributive shockObstructive shock CLASSIFICATION OF SHOCK ACCORDING TO BLALOCKHaematogenic NeurogenicCardiogenicVasogenic

CLASSIFICATION OF SHOCK ACCORDING TO CAUSE Inadequate circulatory blood volume Loss of autonomic control of vasculature Impaired cardiac function77

78Symptoms of shockIncrease heart rate as a result of the baroreflex:Shock will decrease the volume of blood pumped from the heart and the blood flow to the brain. That will activate the baroreceptors in the carotid bodies to increase HR trying to supply enough blood to the vital organs.

Pale skin: As a result of vasoconstriction of the peripheral vessels, because the skin is the least priority tissue for blood flow

79Cold and clammy skin : As a result of vasoconstriction.

Shock decreases the skin surface temperature as a result of vasodilatation, which will increase the internal body temperature. Because the skin plays a major role in controlling body temperature, as it will help in exchanging heat with the external environment.

There are two mechanisms to get red of the excess heat:

Hyperventilation ( Minimal effect in humans)

Vasodilatation of the vessels Flush ( Increase blood flow to the skin) BP Real shock 80

81Initial stage - tissues are underperfused, anaerobic metabolism, lactic acid building

Compensatory stage -Hyperventilation, Baroreceptors, Renin angiotensin axis, vasopressin

Progressive stage - Failing compensatory mechanisms: profound vasoconstriction ISCHEMIA; Lactic acid production is high metabolic acidosis

Irreversible/ refractory stage brain damage , cell death, Multiple Organ Dysfunction Syndrome.

Stages of Shock82

Etiology83

84Hypovolemic ShockClassification of hemorrhagic shock by American College of surgeons committee on trauma (1984)

Class IAcute blood loss 15 % of total blood volume. Pulse & respiration increased. BP not significantly affected.

Class II Acute blood loss of 20 25 % of total blood volume. Increased pulse & respiration. Decreased BP. No decrease in urine output.

Class IIIBlood loss of 30 40 % of total blood volume. Increased pulse & respiration. Decreased BP & Urine output.

Class IV40 50 % loss of total blood volume. Lack of vital signs. Decreased urine output. Obtunded mental status.85Class IClass IIClass IIIClass IVBlood Loss750 ml750 - 15001500 - 20002000 or more% loss15 %15 30 %30 40 %40 % or morePulse rate< 100> 100> 120140 or higherBPNormalnormaldecreasedDecreasedPulse pressure (mm Hg)Normal or increaseddecreaseddecreaseddecreasedCapillary blanch testNormalpositivepositivepositiveRespiratory rate14 2020 3030 - 40> 35Urine output (ml / hr )30 or more20- 305 - 15NegligibleCNS mental statusSlightly anxiousMild anxiousAnxious and confusedConfused & lethargicFluid replacement (3:1 rule )CrystalloidcrystalloidCrystalloid + bloodCrystalloid + bloodHypovolemic Shock86There are three basic compensatory reactions:

adrenergic reaction

Catecholamines

plasma refill

Albumin

acidosisBaroreceptors in right atrium are stimulated and a sympathetic nerve reaction is triggered, resulting in intense stimulation of the adrenal medulla with subsequent release of catecholamines. The basic result is centralization of circulation. In the lungs, catecholamines stimulate the beta2-receptors inducing bronchial muscle dilation. This, associated with tachypnoea produced by acidosis, will increase the alveolar oxygen tension PAO2.

This refill is generated primarily by the decrease of capillary hydrostatic pressure, due to arteriolar vasoconstriction. This will attract protein-free fluid into vascular space. Albumin enters the circulation The increase of colloid pressure attracts free water from extravascular-extracellular space into circulation, increasing blood volume, and redistributing the extracellular fluid.This mechanism alone is responsible for blood replacement in hemorrhages that do not exceed 10% of blood volume.87Hypovolemic ShockOther related compensatory mechanisms are related system wise, and are:

the hematologic systemthe cardiovascular systemthe renal systemthe neuroendocrine systemActivating the coagulation cascade and contracting the bleeding vessels`Increases the heart rate, increasing myocardial contractility, and constricting peripheral blood vessels. This response occurs secondary to an increase in release of norepinephrine. The cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys and away from skin, muscle, and GI tract.

The kidneys respond to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus.

Causes an increase in circulating antidiuretic hormone (ADH). ADH indirectly leads to an increase in reabsorption of water and salt (NaCl)88

89

90 Decompensated shock

I.e. compensatory mechanisms are no longer able to maintain brain perfusion.

The patient is progressively confused, sleepy, and then comatose, as the brain perfusion drops.

Blood pressure is below normal, heart rate is above normal, and radial artery pulse is absent

Skin is pale, cold, patient is covered in cold sweat, core body temperature is decreased, nail bed capillary refill is absent, and patient is anuric.Covert compensated - WHEN BLOOD VOLUME HAS REDUCED BY 10-15 % . NO SIGNIFICANT CHANGE IN THE HR. CO AND SPLANCHNIC BLOOD COMPENSATES FOR THE LOSS.

Overt compensated - HERE PT HAS COLD PERIPHERY, TACHYCARDIA, WIDE ARTERIALPRESSURE, TACHYPNEA, CONFUSION, HYPONATREMIA, METABOLIC ACIDOSIS. BUT STILL SYSTOLIC PRESSURE IS MAINTAINED WELL

91Diagnosis of Hypovolemic ShockThe haemodynamic profile on monitoring of flow pressure variables shows low central venous pressure (CVP), a low pulmonary capillary wedge pressure (PCWP), low cardiac output (CO) and cardiac index (CI), and high Systemic Vascular Resistance. The arterial blood pressure may be normal or low.

elevated potassium, serum lactate, and blood urea nitrogen levels, increased urine specific gravity (greater than 1.020) and urine osmolalitydecreased blood pH and partial pressure of arterial oxygen and increased partial pressure of arterial carbon dioxide.

92ManagementA - B - CActive measures to control bleeding Intravenous Access Drug Therapy - Adrenergic drugsFluid ReplacementIN CASES OF EXTERNAL BLEEDS PRESSURE DIRECT PRESSURE APPLIED. IN CASE OF INTERNAL BLEEDS SURGICAL INTERVENTION IS REQUIRED.

HYPOVOLUMIA SEC TO BURNS ,ACUTE GE. CAN BE TREATED WITH ELECTROLYTE SOLUTIONS THAT BALANCE THE NATURE OF THE FLUID LOST.

A PREGNANT PT SHOULD BE TURNED ON HER LT AS IT TAKES PRESSURE OFF IVC93Fluid TherapyRECOMMENDED - AN INITIAL BOLUS OF 1-2 L OF RINGERS LACTATE IS GIVEN.

BLOOD TRANFUSIONS ARE REQUIRED IF THERE IS A LOSS OF > 20 % OF CIRCULATING VOLUME.

Class I

2.5 L crystalloidsOr1.0 L colloidsClass II

1.5 L crystalloids+1.0 L colloidsClass III

1.0 L crystalloids + 0.5 L colloids + 1.0 L whole bloodOr0.1-1.5 L concentrated red cells + colloidsClass IV

1.0 L crystalloids + 1.0 L colloids + 2.0 L whole bloodOr2.0 L concentrated red cells + 2.0 L colloids94Drug Therapy AgentDoseCardiacHeart rateContractilityDopamineNorepinephrineDobutaminePhenylephrine5-10(/kg)/min.2-20/g/min.5-10(/kg)/min.20-200g/min.

1+1+1-2+0

1+2+3-4+095

96Cardiogenic ShockCardiogenic shock is characterized by a decreased pumping ability of the heart causing a shock-like state with inadequate perfusion to the tissues.

It occurs most commonly in association with, and as a direct result of, acute ischemic damage to the myocardium. Intrinsic

Myocardial injury

Tachycardia

Bradycardia

Valvular defect

Extrinsic

Pericardial tamponade

Tension pneumothorax

Large pulmonary emblous97HistoryMost patients presenting with cardiogenic shock do so in conjunction with an AMI and, therefore, present with the constellation of symptoms of acute cardiac ischemia (e.g., Chest pain, shortness of breath, diaphoresis, nausea and vomiting).

Patients experiencing cardiogenic shock may also present with pulmonary edema and presyncopal or syncopal symptoms.Physical examination will often reveal a patient in the middle of an AMI.

Patients appear in frank extremis, profoundly diaphoretic and complaining of severe shortness of breath and chest pain.

Neck examination may reveal jugular venous distention. This is evidence of rightventricular failure and may be prominent.Cardiogenic ShockCareful attention should be directed toward the cardiac examination, as there are mechanical causes of cardiogenic shock which are readily amenable to surgical intervention, and without which the mortality is dismal. These include papillary rupture, valvular dysfunction, myocardial wall or septal rupture, cardiac tamponade and aortic aneurysm. Loud murmurs may indicate a valvular dysfunction while muffled heart tones with JVD and pulsus paradoxus maysuggest tamponade.98Treatment of Cardiogenic ShockPulmonary wedge pressure (Swan-Ganz Catheter)

Intra aortic balloon pump - An intra-aortic balloon pump is a support device which is inserted in the groin and advanced into the aorta. The purpose is to reduce the workload on the heart.

Preload Fluid administration Inotropic agents :- Dopamine(5-10g/kg/min) ,Dobutamine (5-10g/kg/min), Epinephrine

Afterload Vasodilators :- reduce myocardial wall tension and improve myocardial oxygen supply to demand ratio. Nitroprusside (0.5-5g/kg/min), Nitroglycerine (3 -5 g/kg/min)Optimize cardiovascular function, Improve oxygen delivery Restore tissue perfusion

PCWP 4 - 12 mm of Hg

99

100

Pneumatic Antishock Garment

101Obstructive shockis a form ofshockassociated with physical obstruction of thegreat vesselsor theheartitself.

Pulmonary embolism andcardiac tamponadeare considered forms of obstructive shock.

Obstructive shock has much in common withcardiogenic shock, and the two are frequently grouped together.Obstructive ShockPneumothorax or haemothorax is treated by inserting a chest tube.

Pulmonary embolism requires thrombolysis (to reduce the size of the clot), or embolectomy (removal of the thrombus).

Tamponade is treated by draining fluid from the pericardial space through pericardiocentesisStreptokinase 1.5

Urokinase 2-3102Systemic inflammatory response syndrome :- SIRS to a variety of severe clinical insults. 1) temp > 380 C or < 360 C , 2) HR> 90 beats /min 3) RR > 20 breaths/min . 4) WBC > 12000/cu. mm or < 4000/cu.mm. 5) PaCO2 < 32mm Hg

Sepsis :-SIRS in association with culture proven infectionSeptic shock :- sepsis with hypotension despite adequate fluid resuscitation along with hypoperfusion , lactic acidosis, oliguria, acute alteration in mental statusMultiple organ dysfunction syndrome (MODS) :- presence of altered organ function in an acutely ill patient such that hemostasis cannot be maintained without intervention.Distributive ShockSeptic Anaphylactic Neurogenic103Septic ShockGRAM NEGATIVE SEPTICEMIA (endotoxic shock)E.coli, Klebsiella, MeningiococciGRAM POSITIVE SEPTICEMIA (exotoxic shock)StaphylococcusStreptococci (toxic shock syndrome)Pseudomonas produces both endotoxin and exotoxin 104

105Early warm (hyperdynamic) shock

Fever and chillsHigh respiratory rateProfound diuresis High cardiac outputLow peripheral vascular resistanceArterial blood gas analysis - metabolic acidosis TachycardiaWarm, Dry skinCold (hypodynamic) shockSubnormal temperatureProfound Hypotension and hypoperfusion3. Reduced Cardiac Output 4. Cold and mottled skin5. Rapid pulse and respiration6. Multisystem failure pulmonary edema, ARDS, liver and kidney failure, DIC7. Deteriorated mental status

106InvestigationsUrine Analysis

Nasal & throat swabs

Blood cultures

Sputum specimen

Pus / wound swabs

IV lines/ Indwelling catheter

1071) Ensure a patent airway and that the patient is breathing spontaneously O2 To improve the oxygenation. Oral airway -> ET tube -> tracheostomy

2) Ensure and adequate pulse and blood pressure: Intravenous canulation: volume loading -> inotropes -> inoconstrictors

3) Look for source of sepsis (cultures); assess background issues that may have contributed.

4) Start antimicrobial therapy, guided by cultures, or "best guess therapy

5) ICU staff personal hygeine, to prevent transmission of resistant microbes.

6) Enteral nutrition to prevent bacterial translocation.

7) Low dose steroids (hydrocortisone) for 5 - 7 days : beneficial. However, use of steroids in sepsis is controversial.108DefinitionAn individual response to a specific antigen which is represented by respiratory distress followed by vascular collapse.Predisposing factorsHormones, Enzymes, Polysaccharides (Dextran), Antibiotics, LA.Clinical ManifestationsUpper and lower airway obstruction.Angioedema of epiglottis and larynxAudible wheeze.Non pitting edema.Urticarial eruptions.Anaphylactic Shock

109

Allergic response mediated by IgE antibodyActivation and release of inflammatory mediators anaphylatoxins, C3a, C5a, histamines, kinins, prostaglandins and others.110methylxanthine derivativerelaxes bronchial smooth muscle. Suggested mechanisms are an increase in intracellular cAMP through inhibition of phosphodiesterase; adenosine receptor antagonism, prostaglandin antagonism and effects on intracellular calcium.

111Cricothyrotomyabsolute need for a definitive airway unable to perform ETT due for structural or anatomic reasons, risk of not intubating is > than surgical airway riskunable to clear an upper airway obstruction, multiple unsuccessful attempts at ETT, other methods of ventilation do not allow effective ventilation and respiration112Contraindications (relative)Age < 8 years evidence of # larynx or cricoid cartilageevidence of tracheal transection

113Steroids in Anaphylactic ShockAdminister them early to try to prevent a potential late-phase reaction (biphasic anaphylaxis)

Used as adjunct after initial treatment with epinephrine.

Glucocorticoids can supplement primary therapy to suppress manifestations of allergic diseases of a limited duration.

In very severe diseases intravenous methylprednisolone 125mg every 6 hours

Patients with asthma may receive additional benefit if corticosteroids are administered to them during anaphylaxis.114Anaphylactoid ReactionA reaction that resembles anaphylactic shock; probably caused by the liberation of histamine, serotonin, or other substances as a consequence of the injection of colloids or finely suspended material.

Unlike, anaphylaxis it is not IgE mediated.

However, the treatment for both is essentially the same.115Neurogenic ShockOccurs when sympathetic denervation produces an impairement in vasomotor tone Etiology

Spinal anesthesia Brain damage Sudden onset of pain Clinical features

Hypotension Bradycardia Extremities are warm and dryFainting is variation of neurogenic shock116Pathogenesis

Sympathetic denervationImpaired vasomotor tone (arterial & venous system) systemic vascular resistance venous return to heart cardiac outputSHOCK117Management

Morphine 15mg i.m. should be given

Balanced salt solution to increase cardiac output

Vasopressor drugs dopamine 200mg i.v. infusionmephenteramine 30-60mg i.v.

Body temperature should be monitored to prevent hypothermia and minimize effect of shock118Endocrine ShockHypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.

Thyrotoxicosis - may induce a reversible cardiomyopathy.

Acute adrenal insufficiency (Addisons) is frequently the result of discontinuing corticosteroid treatment without tapering the dosage.Stress

For chronic adrenal insufficiency, the major contributors areautoimmune adrenalitis,tuberculosis,AIDSandmetastaticdisease.Minor causes of chronic adrenal insufficiency aresystemic amyloidosis,fungal infections,hemochromatosisandsarcoidosis.119Clinical features

Malaise, weakness, wt loss, anorexia, nausea, vomiting, diarrhoea

Abdominal tenderness and fever

Hyperpigmentation

Hypotension

Hyponatraemia

HyperkalaemiaHypoadrenal Shock 120121 PrognosisThe prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse122

123Shock, whatever the cause, is associated with an imbalance in oxygen supply and demand.

Early aggressive treatment with oxygen, fluid administration, and adrenergic agents when needed, combined with methods to correct the underlying cause, help to limit the damage.

Repeated clinical examination, with appropriate hemodynamic and oxygenation parameters, is important to monitor the patients progress and response to treatment.

The development of improved monitoring techniques, including strategies to visualize and quantify microcirculatory changes, will enable us to better assess and target regional perfusion; and by so doing, improve patient outcomes.Conclusion124References

Bailey and Loves - Short Practice of Surgery

Harrisons - Principles of Internal Medicine

Schwartz Shires Spencer - Principles of Surgery

Concise text book of surgery - S. Das

Sreenivasan B. - Textbook of Oral and Maxillofacial Surgery

Essentials of Pharmacology - K.D. Tripathi

Rowe & Williams - Maxillofacial Injuries Vol. I

The Internet

125

ThankYou126PATHOPHYSIOLOGY OF SHOCKcardiac output arterial pressure systemic blood flow cardiac nutrition nutrition toIntravascular tissues clotting nutrition tissue nutrition toto brain ischemia vascular system vasomotor Release of toxins capillary permeability activityVasodilationVenous poolingCardiac depression Venous return1Renin-Angiotensin-AldosteronePlasmavolume [Na+]Kidney(juxtaglomerularapparatus)Detected byReleasesReninAngiotensinogenAngiotensin IConverts&/OrVia ACE(AngiotensinConvertingEnzyme)Angiotensin II

1Renin-Angiotensin-AldosteroneAngiotensin II

vasoconstriction PVR BP! thirstFluidvolumeADH(anti-diuretichormone)AdrenalcortexReleasesAldosteroneNa+reabsorption1The end point of successful resuscitation includes:

1. Urine output of > 1 ml /kg/Min.2. Reappearance of peripheral pulses, with adequate MAP and pulse pressure.3. Return to near normal of heart rate.4. Correction of hypothermia, with reduction of core to peripheral temperature gradient to < 1 C.5. Capillary refill < 3 sec.6. Correction of metabolic acidosis with normalization of pH.1Nidus of InfectionOrganismOrganism ToxinsEndotoxin ExotoxinCytokinesPAFArachidonic acid metabolitesComplements and coagulationMDSHistamineMyocardiumDepressionDilationVasculatureVasodilationEndothelial destructionMaldistribution of blood flowDepressed COHypotensionSVR Perfusion failure MOFS - death1

1