Set Up and Use of the Anesthesia Machine

Intubation Tips.mpg

Horse Shoeing

VSR-511 Class Three

Hygroma of Knee:

It is the synovial swelling over the dorsal surface of the carpus.

Mostly acquired bursitis from trauma.

The tendon of the sheath of extensor carpi radialis or common digital extensors may be involved.

A synovial hernia of the antebrachiocarpal or mid carpal joint capsule can occur.

Acquired bursitis shows an evenly distributed swelling over the surface of carpus.

Etiology:

Trauma, exercise on hard ground, hitting carpus on the wall.

Signs:

Swelling on the dorsal surface of the carpus.

Diagnosis:

Explore by needle to drain the fuild for cytological exam.

In Acute Hygroma – serous type of fluid, and in chronic case synovial type of fluid.

Treatment:

Injection of corticosteroids followed by elastic bandage counter pressure 3-5 times at weekly intervals.

In acute cases ,drainage by 4 cm vertical incision , fibrin removed from inner surface with 3 % iodine with penrose drainage.

Open-Knee:

Irregular profile of the carpal joints when viewed from the side.This shows as if carpal joints are not fully closed. This is in young horses (1-3yrs of age ), accompanied by epiphysitis.This is weak confirmation leading to carpal injury.

Bleemish Knee:

1.Backward (palmar) deviation of carpal joints ( CalfKnee or Sheep Knee)

Weak confirmation, seldom sound under heavy work.

Strain on carpal and radial check ligaments, and proximal,middle and distal accessory carpal and palmar carpal ligaments.

Palmar reflection of the antebrachiocarpal joint capsule.

Increased compression on the dorsal aspect of the carpal bones.

Chip # of 3^rd ,radial and intermediate carpal bones common and small chip # of radius.

2.Forward (Dorsal) deviation of the carpal joints(Bucked knees or knee sprung) also goat knee or over in the knees.

By contraction of the carpal flexors, i.e., ulnaris lateralis, flexor carpi ulnaris, and flexor carpi radialis.

Extra strain on sesamoid bone, the superficial flexor tendon, extensor carpi radialis and suspensory ligament.

Forward deviation of carpal joints may be accompanied by enlarged epiphysis or distal metaphysis of the radius.

3.Medial deviation of the carpal joints(Knock knees)

4.Lateral deviation of the carpal joints(Bow legs)

5.Tied in knees:

When viewed from the side, the flexor tendons appear to be too close to the cannon bone just below carpus and ventral aspect looks as if notched.

6.Cut out under knees:

Cut out appearance just below the carpus on the dorsal surface of the cannon bone. It is fundamentally weak conformation.

Fracture of carpal bone:

Common in race horses, young thorough breds of 2-4 years of age.

Factors disposing for fracture are speed, immaturity, longer limb length, position of jockey, distances run which generate tremendous concussive forces on dorsal surface of carpal bones.

Fractures can be simple chip fractures, slab fracture or comminuted fracture.

Most common sites of fracture are radial, 3^rd, intermediate carpal bones and distal end of radius.

Collateral fracture by weigth on one side because of the # in another side.

Counter clock wise direction of racing by position of rider leads to chip # of right forelimb, and by clock wise direction racing left forelimb chip #.

Slab # extends through full thickness of the bone from proximal to distal, commonly 3^rd, intermediate and radial carpal bones.

Communited # commonly radial, intermediate and 4^th carpal bones.

Etiology of the # of carpus:

1.Trauma from repeated concussion and external blows.

2.Fatique creates abnormal compression on the dorsal surface of the carpal bones.

3.Faulty conformation leads to calf kneed predisposed to carpal #.

4.Improper trimming and shoeing result in imbalanced foot and unequal distribution of weight will affect carpus.

Signs:

Intra-articular chip # within carpus result in varying degrees of heat, pain, joint distension and lameness.

By physical exam, synovial distension of the antebracheal(radiocarpal) joint or mid carpal joint.

In acute chip fracture, synovitis is diffuse at first, eventuallybecome more localized in soft tissues over chip fracture, over dorsomedial surface of the carpal joints.

By 3^rd carpal bone fracture, swelling is seen on mid carpal joint.

Degree of lameness depends on extent, location, duration of the fracture and the amount of degenerative joint disease.

The assessment of the degree of carpal flexion and the carpal flexion test can be valuable tools in the diagnosis of carpal lameness.

Palpation of the dorsal border of each carpal bone in both joints is important diagnostic tool.

Diagnosis:

Carpal lameness confirmed by intra-synovial anaesthesia, by injecting 5-10ml of local anaesthetic into antebrachiocarpal or midcarpal joints after equal amount of synovial fluid removed.

If the fluid withdrawn is homogenous dark red fluid, no local anesthetic to be given, as it could be a #.

After 20-30min of injection, lameness is reevaluated.

Treatment:

Chip Fracture: Decide for conservative management or surgical removal.

Selection of treatment depends on physical findings, the size and shape of the chip and its location.

Small Chip # are firmly attached to parent bone are handled conservatively with a period of rest.

On physical exam they will show mild pain and lameness.

For large acute chip # with displacement and free floating that affects weight bearing, treat only by surgery.

Joint more painful on flexion/palpation.

Arthroscopy allows to remove chips without arthrotomy.

NSAIDS to reduce acute inflammatory process.

Intrasynovial sodium hyaluronate reduces synovitis, progressive cartilage destruction and formation of osteophytes.

After chip # is removed, pressure bandage for 3-4 days, Antibiotics and phenyl butazone for 7 days.

Accessory carpal bone fracture:

Most common in thorough breds, show jumpers.

Most common fracture in vertical plane through lateral groove formed by long tendon of ulnaris lateralis muscle.

The pull of the flexor muscles results in a constant distraction and the instability with movement results in a fibro cartilagenous nonunion.

Etiology:

1.Direct external trauma from a kick.

2.Asynchronus contraction of flexor carpi ulnaris and ulnaris lateralis muscles.

3.Bow string effect of flexor carpi ulnaris & ulnaris lateralis muscles and flexortendon created when horse lands on a partially flexed forelimb.

4.Bone caught between 3^rd metacarpal and radius in a nut cracker fashion.

 

Signs:

Signs of lameness not acute.

Most prominent sign of lameness is distension of carpal sheath, marked pain with rapid flexon of the carpus.

Abnormal lateral and  medial movement of the accessory carpal bone.

Diagnosis:

When carpal sheath is distended, pain on flexion, lateral radiograph will show up fracture.

Treatment:

Three types of treatment.

1.Conservative treatment—Rest in box stall for 3-6 months.

2.Internal fixation by lag screw principal. Two 4.5 mm ASIF screws for interfragmentary compression of the fracture.

3.Removal of the fracture of accessory carpal bone for  vertical fracture and ulnar neurectomy.

Carpal hyperextension and carpal arthrosis observed.

Prognosis:

Guarded dependent on fracture, duration and method of repair and intended use of horse.

Good result by internal fixation for interfragmentary compression.

Contracted flexor tendons (knuckling at the fetlock)

Three degrees of the condition.

1.The phalanges are almost vertical.

2.Perpendicular let fall from the front of the fetlock, strikes the front of hoof.

3.Striking in front of hoof.

 

In young animals—

Cause:

Insufficient nutrition to dam.

Muscular debility by confinement to stable.

Insufficient food.

Digestive troubles.

Muscular rheumatism

Rickets.

The condition more in front legs.

In muscular weakness, patient stands over knees.

Symptoms:

Complete flexion of affected joints or some degree of flexion.

Horse stumbles when trotted, leading to open wound and septic arthritis.

Prognosis:

Congenital – recovers easily.

Acquired – due to some systemic defect, prognosis guarded.

Treatment:

Aim of treatment is to make toe of the foot to bear weight.

Splints/POP bandage to maintain foot in position.

Friebels apparatus to keep fetlock in position and application of sling for easy recovery.

In Adults—

Cause:

1. Excess flexion by tendon contraction folloeing chronic tendinitis.

2.Shortening of structures by ring bone,  osteoperiostitis of pastern, chronic synovitis, contracted foot and corn.

      

 

 

 

 

WOUND

Wound:

Definition:  A break in the continuity of soft tissues by trauma or surgery.

Classification:

Closed wounds (No break in the continuity of skin or mm but underlying tissues damaged)			Open wounds (Break in the continuity of skin)
Contusion ( By blunt objects, damage to skin or  S/C tissue without break in skin surface) According to the severity and extent of tissue damage: 1.First degree with rupture of capillary vessels of the skin and subcutaneous tissue. 2.Second degree with rupture of larger vessels leading to haematoma formation. 3.Third degree with major damage of tissues leading to gangrene formation.	Bruise (Mild degree of contusion, characterised by rupture of skin capillaries giving reddish blue to purple colour)	Haematoma (Collection of blood in abnormal cavity, by injury to superficial vein in s/c or submucous) Eg: Cattle-Mammary Vein. Horse-External thoracic vein by rider. Dog-Ear flap	1.Incised wounds 2.Lacerated wounds 3.Punctured wounds 4.Penetrating wounds 5.perforating wounds 6.Gun shot wounds 7.Abrasions 8.Avulsions 9.Aseptic wounds 10.Contaminated wounds 11.Infected wounds 12.Granulating wound 13.Ulcerating wounds 14.Bite wounds 15.Virulent wounds

 

·   Incised wounds are caused by sharp cutting instruments such as knives, scalpels, fragments of glass etc with minimum loss to tissue, edges are regular, bleeds freely and painful, heals by first intention.

·   Lacerated wounds are caused by tearing of tissues with torn and uneven edges. Wounds have irregular jagged borders and loss of tissue is limited to skin and subcutaneous tissue e.g.: barbed wire.

·   Punctured wound are caused by sharp pointed objects like nails relatively with a small opening. There might be presence of infection/ foreign particles deep into the wound with inadequate opening for drainage. Ex: Stab wounds.

·   Penetrating wounds are types of deep wounds communicating with cavities like abdomen, thorax, and joints etc. e.g.: stab wounds.

·   Perforating wound is having two opening, one of entrance and other of exit.

·   Gunshot wound is produced by various forms of firearms e.g. injuries caused by bullet.

·   Abrasions are superficial damage to the skin, generally not deeper than the epidermis.

·   Avulsion occurs when an entire structure or part of it is forcibly pulled away. Eg: Horn or Hoof avulsion.

·   Aseptic wound is surgical wound made under aseptic conditions where chances of bacterial contamination are negligible.

·   Contaminated wound is one where there is presence of micro organisms.

·   Infected/ septic wound: A contaminated wound may become infected after a period of 6 -8 hours where bacterial multiplication may occur and liberation of their toxin.

·   Granulating wound is one in which there is a tendency to heal within expected time.

·   Ulcerating wound have no tendency to heal like horn cancer or cancer wounds.

·   Bite wounds are caused by snake; dog or wild animals bite with significant degree of tissue damage.

·   Virulent wounds are caused by bacteria or virus leading to formation of pustules or vesicles e.g.: FMD, anthrax.

Symptoms:

Local	General	Remote
1.Haemorrhage 2.Gaping of wound edges 3.Pain 4.Repair phenomena	1.Febrile disturbance by virulence of infected organisms and degree of injury to tissues and toxemia.	Symptoms observed away from wound part. Abscess formation in dependent lymph gland, paralysis or loss of sensation in the dependent part or neuritis.

 

Healing of an wound:

1.First intention healing-(Primary union)

For primary healing

The wound should be

Clean and fresh wound,

Free of infection,

 No hemorrhage,

No foreign bodies like nails or thorns,

Minimal dead cells,

 Good blood supply to wound edges,

 the part should be given rest by immobilization in which different layers of tissues are properly aligned.

Narrow space between wound edges are filled with blood clot.

Capillaries and fibroblasts grow into this from wound edges and healing completed in 5-14 days.

Little scar tissue is formed.

By 3^rd day, capillaries proliferate in the wound, By 4^th day, fibroplasias is evident.

After fibroplasias, wound has tensile strength, in 10-14 days sufficient tensile strength is obtained.

2.Second intention healing: (Healing by granulation)

By replacement of tissues

In wounds with extensive loss of tissues and edges widely separated.

Granulation tissue has budding capillaries and fibroblasts grow from edges and the bottom of the wound to fill the gap.

Granulation tissue is highly vascular, velvety, soft, moist and pink in appearance, these capillaries grow up and anastamose forming network.

Fibrous tissue proliferates and fibres are interlaid among the capillaries.

Fibrous tissues and capillaries will come to the surface of the wound and surface epithelium also grows from its borders and healing gets completed.

Fibrous tissue contracts causing constriction of capillaries giving pale colour to scar tissue/Cicatrix.

By 2^nd intention healing happens in 14-21 days.

3. Mixed intention healing:

Sutured wound partially disturbed, which heals partly by 1^st intention and partly by 2^nd intention.

4.Third intention healing-(Healing by 2^nd suture)

When granulating surfaces have to heal by 2^nd intention, unite them by sutures to bring quick healing.

 

 

5.Healing under a scab:

In superficial wounds like abrasions, exudates in wound dries up and forms a scab. Under the scab healing process(granulation) takes place, scab automatically separates and falls off.

 

·   The Four phases of wound healing are

• Haemostasis
• Inflammatory phase
• Proliferative phase
• Wound remodeling

·         Haemostasis:

·         The initial vascular response involves a brief and transient period of vasoconstriction and hemostasis.

·               A 5-10 minute period of intense vasoconstriction is followed by active   vasodilatation accompanied by an increase in capillary permeability.

·               Platelets aggregated within a fibrin clot secrete a variety of growth factors and cytokines that set the stage for an orderly series of events leading to tissue repair.

• Inflammatory phase:
• The second phase of wound healing i.e. the inflammatory phase lasts for 1-3 days in uninfected wounds.
• The inflammatory response increases vascular permeability, resulting in migration of neutrophils and monocytes into the surrounding tissue. The neutrophils engulf debris and microorganisms, providing the first line of defense against infection.
• In the late inflammatory phase, monocytes converted in the tissue to macrophages, which digest and kill bacterial pathogens, scavenge tissue debris and destroy remaining neutrophils. Macrophages begin the transition from wound inflammation to wound repair by secreting a variety of chemotactic and growth factors that stimulate cell migration, proliferation, and formation of the tissue matrix.

         Proliferative phase

        The subsequent proliferative phase is dominated by the formation of granulation tissue    and epithelialization.

o    Chemotactic and growth factors released from platelets and macrophages stimulate the migration and activation of wound fibroblasts that produce a variety of substances essential to wound repair, including glycosaminoglycans (mainly hyaluronic acid, chondroitin-4-sulfate, dermatan sulfate, and heparan sulfate) and collagen.

o    These form an amorphous, gel-like connective tissue matrix necessary for cell migration.

· New capillary growth must accompany the advancing fibroblasts into the wound to provide metabolic needs.

o    Collagen synthesis and cross-linkage is responsible for vascular integrity and strength of new capillary beds.

o    Around the third day after wounding the growing mass of fibroblast cells begin to synthesize and secrete measurable amounts of collagen.

o    The amount of collagen secreted during this period determines the tensile strength of the wound

Wound remodeling

·   The final phase of wound healing i.e. remodeling develops 3 weeks following injury and continues up to two years.

·   This phase is characterized by reorganization of new collagen fibers, forming a more organized lattice structure that progressively continues to increase wound tensile strength.

·   The strength of scar tissue formed in this phase is less than the surrounding normal tissue

Factors for delay in wound healing:

1.Improper apposition or dead space.

2.Bacterial infection.

3.foreign bodies like thorns,metal pieces.

4.Devitalization of tissues of wound edges by

a) Lack of blood supply

b) Old age

c) Deficiency of Vitamins like A,D,B-Complex.

d) Dessication of tissue by drying.

e) Overhydration or edema.

f) Malnutrition especially Protien and Glucose.

h) Defi. of Vit C for collagen formation.

i) Defi. Of Vit K for coagulation of blood.

j) Chemical and mechanical trauma.

5. Haematoma/Serum Collection , media for bacteria proliferation.

6. Malignant neoplastic tissue.

7.Lack of immobilization—rupture of newly formed granulation tissue.

8.Presence of dead tissue—debridement is necessary.

Treatment of wounds:

1.Closed wounds:

a)Contusions treated by cold astringent application to minimize extravasation.

(Mag sulf+Glycerine or Creata+Acetic acid)

b) Haematoma-Small one will be absorbed, Large should be opened and treated.

2.Open wounds

For Aseptic wounds-

a)Control Bleeding

b)Sutured for 1^st intention healing.

For Contaminated wound

a)Control bleeding by ligating larger blood vessels.

b)No sutures to be applied for infected wounds

c)Clean the wound by clipping the hair and irrigating with mild,nonirritant antiseptic lotion to remove dirt and dead tissue by 5-10% hypertonic saline solution or 1 in 500 acriflavin solution or by Hydrogen peroxide application.

d) Foot lesions treated with 10 5 formalin foot bath.

4.Control of infection:

Dry wounds—Ointments like Boric or iodine oint or BIPP.

Wet wounds—Powders like Boric or Eupad(Bleaching powder+Boric powder) or sulphanilamide powder.

Antibiotics parenterally.

Tetnus toxoid for horses and goats is essential.

5.Drainage of wounds: ( Sterilized guage/capillary tube/perforated tube)

Pen rose drains for deep wounds to remove tissue exudates/discharges.

6.Immobilization of a wounded area:

If wound is not immobilized, excess granulation tissue ( proud flesh) is formed in wounds below knee/hock joint.

Powdered caustic like Copper sulphate/Potassium permanganate is applied on wound with pressure bandage for 48 hrs and checked for removal of granulation tissue, if not removed then surgical removal is advised.

 

Complications of the wounds:

1.Severe haemorrhage leading to shock

2.Traumatic neuralgia

3.Traumatic emphysema

4.Venous thrombosis and embolism

5.Traumatic fever

6.Erysepelas

7.Septicaemia and pyemia

8.Gas gangrene

9.Tetanus

10.Other infections

11.Adhesions between adjacent structures during healing of the wound.

1. Hemorrhage:

Bleeding from a wound, if larger vessel is wounded no coagulation takes place.

In deficiency of Vit K and Calcium.

By heredity—Haemophilia/Leukemia. Or diseases of liver/heart/blood vessels.

Continuous bleeding leads to shock

Syncope (fainting) by cerebral anaemia and unconsciousness by sudden fall in BP and active vasomotor depression.

Cardiac and respiratory inhibition , and muscle relaxation leads to death by heavy bleeding.

2.Traumatic Neuralgia:

By traumatic injury, severe pain along the course of the nerve is neuralgia.

Primary neuralgic pain starts ever since wound is produced.

Secondary neuralgia pain after few days after wound by pressure and subsequent infection.

Treatment:

Clean the wound with antiseptic lotion.

Anodyne and antiseptic dressing is applied.

Warm and moist fomentation and administration of NSAIDS.

3.Traumatic emphysema:

Emphysema is infiltration of tissue spaces with air.

It is common complication of punctured wounds of respiratory tract and alimentary tract and also punctured wounds of axilla and groin and peri-articular tissues.

During movement air gets trapped in wound and spreads into subcutaneous tissue and forms emphysematous swelling.

Air from digestive tract can give infected emphysema.

If it involves extensive area it may cause general discomfort and dyspnoea.

Treatment: Apply pressure and remove the air through wound and antibiotics.

4.Venous thrombosis:

By injury to a vein at the site of the wound, thrombosis is formed, which may break in vein and curved forward in the blood stream as emboli.Emboli if larger can block pulmonary artery, coronary artery and arterioles in brain producing instant death. Septic emboli can cause general septicaemia.

5.Traumatic fever:

The rise of the body temperature by wounds. Fever  can be produced post operatively also.

Rise of temperature is due to reaction of tissue to the trauma. Fever is characterized by high temperature, pronounced leuckocytosis and neutrophilia.

Persistant fever by secondary bacterial infection requires antibiotics administration.

6.Erisepelas:

By infection of the wound by streptococcus infection in horse and dogs. Erisepals in pigs by E.Rusiopathae,it is cutaneous form.

In 3 forms a) Cutaneous form-Diffuse, hot painful swelling of skin,spreads rapidly with high temperature and lymphangitis.

b)Phlegmatous form-Diffuse suppurative lesions.

c)Gangrenous form-Extensive gangrenous lesions seen.

7.Septicaemia and pyaemia:

Pus in general circulation, so profound depression in general condition and febrile condition. Antibiotics are used.

8.Gangrenous septecaemia(Gas gangrene)

Infection of wound with gas producing bacteria.

Hot painful, edematous swelling develops surrounding the wound, spreads rapidly, putrefactive changes give foetid gas and grayish red discharge.

High temperature followed by subnormal temperature, toxic symptoms are seen.

 Incurable after toxic symptoms develop.

9.Tetanus:

Disease caused by infection of wound by clostridium tetani by anaerobic fermentation, releasing toxins like tetnospasmin and tetnolysin. Produces titanic convulsions.Develops 3 days to 3 weeks after castration /docking.

10.Other infections:

Wound may be infected by other organism like actinomycosis/actinobacillosis, BQ, Anthrax, fracy etc.

11.Adhesions:

Open wound with muscles and tendons form adhesions ,will cause  difficulty in  movement leading to lameness.

Maggot wound : (Traumatic Myiasis)

It comes from greek word Myia=fly.

Myiasis—Condition caused by infestation of the animal body by flies or their larvae(maggots).

Classification:

Primary	Secondary
1.Flies with habit of breeding only in wounds of warm blooded animal.	1.Flies complete lifecycle without larva in wound of warm blooded animals.
2.larvae from eggs burrow deep into tissues	2.Donot burrow deep.
3.They feed on living tissue.	3.Feed on necrotic tissue.
Eg: Lucilia Cuprina(Green bottle fly)       L.Sericata       Calliphora Erythrocephala(Blue bottle fly)       C.Vomitora       Phoromia sps.	Eg:Chrysomia Bezziana       C.Chloropya       (Bluish green bottle fly)       Sarcophaga Haemmorhdalis       Musca Domestica(Common house fly)

 

Life Cycle:

Lifecycle of flies causing myiasis takes about 21 days

Egg deposited in wound hatch in one day àLarva 6 day growth phase àDropped on soil àpupa àAdult (8day to 21months)                  

Prognosis:

Primary myiasis: If not treated, death in 2 weeks in fly seasons with repeated infestation àmore dangerous in sheep, goats and horse then in cattle.

-Within 4 days infection gets treated but requires one month for recovery.

Secondary myiasis gets treated easily.

Mixed myiasis is possible.

Treatment:

1.Chloroform, turpentine, camphor in oil for 24 hrs in guage.

2.Open wound treated with fly repellents like neem oil, loraxane(Proflavin), Annona squamosa leaves.

3. Inj.Ivermectin will relieve maggots fastly.

Maggots in greek medicine—Keeps wound in alkaline medium, bacteria in acidic medium so no pus in maggoted wound.

 

Surgical bacteriology of wounds:

Infection through wounds is called surgical infection.

Application of knowledge of bacteriology for diagnosis and treatment of surgical infections called as surgical bacteriology.

Bacteria responsible for wounds are

1.Staphylococcci, 2.Streptococci, 3.Bacillus Coli, 4.Bacillus Pyocyaneus.

1.Staphylococci—S.aureus,S.albus, S.Citras –Produce frank pus, abscess with thick creamy pus.

2.Streptococcus—No frank pus, Inflammation like cellulitis, swelling spreading more extensively, no abscess but thin watery and scanty discharges.

3.B.Coli-G.I tract commensal, thin watery pus with offensive odour.

4.B.Pyacyaneus-In mixed infection with green colour pus.

Animal Bite wounds:

Dog bite	Scorpion sting	Snake bite	Insect bite	Rat bite
Rabid/Not	Severe pain , burning sensation, 4-6 hrs profuse sweating,gasping, anaphylactic shock.	Cobra and krait are neurotoxin. Krait –painless bite. Viper-Cardiotoic or hemotoxic	Wasp,Bees,Spiders-produces local infl and urticaria.	Intermittent fever(Rat bite fever) in humans. By Spirochetes(Spirullinum minus).
Observe for 10 days	In 10 vomiting blood with pulmonary edema.	Treatment: Polyvalent Antivenom	Treat: Wash with alkaline Solun. Sting should be removed. Corticosteroids for urticaria.
Soap water	Death in 2-3 days
	Treatment: Symptomatic Salines, Corticosteroids, Atropine, morphine.