LIGHTNING STROKE. ELECTRIC SHOCK.

Fatal. Non-fatal. Herbivora at pasture under tree. Symptoms: dazed for

a few minutes, unconscious for hours, permanent paresis or paralysis.

Lesions: lines of burned hair, skin or muscles, rigor mortis slight,

decomposition rapid, bluish black venous and capillary congestion,

extravasations, blood fluid. Diagnosis. Treatment: ammonia, ether,

alcohol, caffein, nerve stimulants.

While a stroke of lightning is usually fatal, yet in certain cases, the

victim is but temporarily stunned and recovers with more or less

remaining paralysis. The subject has also great importance in connection

with the claim of the owner against a company which may have insured his

stock against lightning.

Any animal may be struck, but the herbivora which are turned out to

pasture are especially liable to such injuries, because they seek

shelter under trees, which operate as lightning rods.

_Symptoms._ In slight cases of shock whether by lightning or the current

of a hanging live electric wire, the subject may be simply dazed and may

or may not fall to the ground, and recover itself in a very few minutes.

In other cases there is a more violent shock which prostrates the animal

to the earth, where it may lie unconscious for some hours and yet

quickly and completely recover. In still other cases after such

prostration recovery is incomplete and the animal remains affected with

paresis or paralysis of one or more, commonly of both hind, or all four

limbs. In the more violent shocks death is instantaneous.

Often the impact and course of the current are marked by visible

lesions. Sometimes the skin is wounded exposing a bluish black tissue

beneath. More commonly there is an area of burnt hair, or straight,

radiating or angular lines of raised and frizzled hair marking the

course of the current. In a horse killed by an electric light wire in

Ithaca recently the current had burned to a depth of several inches in

the muscles of the shoulder which rested on the wire.

_Lesions_ are often rather indefinite. There may be no appreciable

change in the nervous system. Rigor mortis is slight; it passes off

rapidly and decomposition sets in early. The venous system and

capillaries are usually filled with liquid blood of a dark bluish black

color, and at intervals are points, spots and patches of blood

extravasation. The uniformly liquid state of the blood is one of the

most marked phenomena of death from electricity. The dark blue

congestion of the radical veins is also very pathognomonic, the part

struck or traversed by the main current, being the seat of the most

elaborate arborescent network. This arborescent appearance of the dark

colored veins, and the petechiæ are often marked in the internal organs

(brain, kidneys, liver, lungs).

_Diagnosis._ The environment of the animal will often clear the

diagnosis. The patient is found helpless, or dead under a tree, by a

pole, or under a hanging wire, and if a tree there are evidences of the

electric shock in scattered leaves and branches, stripping off of the

bark, or perhaps rending of the tree in pieces. In case of wires

attached to or passing near such a tree, the supporting poles show

similar splitting and rending. Add to these the fluidity of blood in the

carcase, the thickly ramifying network of the minute dark bluish, red

veins, the petechiæ and the comparative absence of cadaveric rigidity,

and we have a picture very significant of lightning stroke.

_Treatment_ in such cases is according to the condition. The primary

unconsciousness is met by inhalations of ammonia or ether, or the

injection of brandy or alcohol subcutem. Caffein, atropine or hyoscyamin

may be used as substitutes. If consciousness returns recovery is usually

rapid and complete. Should paresis or paralysis remain it must be

treated like any ordinary case of these affections.

INTRACRANIAL HÆMORRHAGE AND THROMBOSIS. APOPLEXY. SOFTENING OF THE

BRAIN.

Definition. Causes: Nature: intracranial rupture, with pressure,

serous effusion, excessive congestion, experimental cases, anæmia from

pressure, comparative immunity of horse, heart disease, Bright’s

disease, atheroma, degeneration, emboli, age, blood tension, severe

exertion, excitement, concussion, insolation, venous obstruction,

toxins, neoplasms. Lesions: blood clots, small and multiple, large and

solitary, brain absorption, cavities, cysts. Symptoms: dullness,

swaying, trembling, elevation of head, turning in circle, sudden fall,

spasms, unequal dilated or contracted pupils, eyes turned to affected

side, congested or anæmic mucosæ, stertor, puffing cheeks except in

solipeds, pulse slow, soft, full, vomiting, stupor, coma,

unconsciousness, paralysis, monoplegia, hemiplegia, sequelæ.

Diagnosis: sudden unconsciousness, with little spasm, but paralysis,

history, sign of trauma, deep coma, eyes turned to one side, pupils

unequal, stertor, slow breathing and pulse; from uræmia, pulmonary

apoplexy, œdema or anthrax. Treatment: bleeding, ice pack, snow, cold

water, rest, derivatives to limbs, later purge, bromides, potassium

iodide, tonics, open air life.

_Definition._ Cerebral apoplexy has been defined as a sudden loss of

sensation and voluntary motion, from pressure originating within the

cranium and followed by paralysis, often unilateral. The definition is

somewhat insufficient as regards the early symptoms as the same

conditions attend on convulsions and epilepsy (haut mal), and it is only

by excluding these by their characteristic features of sudden seizure

with clonic spasms and their intermittent and paroxysmal habit that we

reach an easy and satisfactory distinction. Later the paralysis tends to

identify the apoplectic attack.

_Causes and Nature._ The immediate cause and essential lesion of

apoplexy has been generally held to be the rupture of an intracranial

artery and the formation of a considerable blood clot which presses upon

(and abolishes the functions of) the brain. There are cases, however, in

which the characteristic symptoms are present, and yet a complete

recovery ensues at an early date, too early to allow for the absorption

of a considerable clot. Moreover, in fatal cases perhaps no blood clot

is to be found, but in place a serous effusion, or an internal

congestion which exercised the fatal pressure on the brain. So far,

therefore, as clinical phenomena are concerned, we must allow that

apoplexy may arise from any sudden pressure on the brain substance.

Pagenstecher produced the symptoms of the disease by injecting, at a

regulated pressure, melted wax and tallow between the skull and dura

mater in the dog. In the moderate cases there were drowsiness, psychic

depression and general muscular weakness. In the more severe ones there

were added sleep and unilateral paralysis. In the more extreme cases

death followed in a few hours after coma set in, though in some of these

a partial recovery ensued if the waxy mass was scooped out before the

fatal symptoms appeared. Cases ended fatally only when the injection

pressure equalled that of the blood, and convulsions occurred only when

the pressure was unsteady. The temperature fell as it does in apoplexy

in man, at the outset, but it continued falling to the fatal issue

contrary to what takes place in man.

Duret injected water into the cranium of animals so as to produce great

tension of the occipito-atloid membrane causing thereby arrest of the

respiration and slowing of the heart’s action. On tearing the membrane

so as to allow escape of the water, respiration began anew and

consciousness was gradually restored.

Edes sustains the view that apoplexy is directly due to anæmia of a

lesser or greater portion of the brain substance, and that this need not

be in any one particular seat nor of any definite extent. This anæmia is

usually induced by pressure and may be caused by effused blood, or

serum, or by the extreme congestion due to narcotic poisons, or other

cause. Embolism of a cerebral vessel, however, by cutting off the blood

from the part of the brain which it supplies may give rise to the

apoplectic phenomena.

Friedberger and Fröhner found apoplexy quite frequent in sheep, ox. and

dog, and rare in the horse, although more subject to the violent

exertion which they put in the front of all causes. It is probable that

the sluggish, pampered life of the first three animals, and the tendency

to fatty degenerations and heart disease introduces a special

predisposition as it does in man, while the horse, inured to an open air

life and a vigorous muscular condition, is comparatively immune.

Bright’s disease is a common cause in the human subject, with its

resulting cardiac hypertrophy. The degenerations attendant on these

conditions and especially fatty change (atheroma) in the walls of the

cerebral arteries, pave the way for their rupture and for blood

effusion. Emboli also carried from the diseased heart not only cut off

the blood from the parts supplied by the plugged arteries, but increase

the blood tension on the cardiac side of the obstruction and endanger

rupture at any weak part. Thus they may cause apoplexy from anæmia

without rupture or apoplexy from the pressure of effused blood.

=Age= which is such a notorious factor in man is not without its

influence in the lower animals. It is in the old that we mostly see

disease of kidneys and heart and the degenerations of the tissues,

including the brain and its vessels; in these, therefore, rupture and

extravasation are the most frequent.

The other causes are mostly connected with increased blood tension with

or without a debility of the vascular walls. Violent exertions as in

racing, coursing, dragging heavy loads up hill or on heavy ground,

severe excitement, cerebral concussion, insolation, and intense

congestion of the brain substance have all been recognized as causative

factors. The compression of the jugulars by a small collar, the violent

straining attendant on parturition, or constipation, and even the

retrocession of blood from the surface when exposed to extreme cold, may

contribute to the final rupture.

In infectious diseases in which the toxic products tend to produce

profound modifications in the blood and tissues, extravasations are met

with in the brain as in other organs. Thus they are seen in anthrax,

Texas fever, petechial fever, etc.

Then the formation of =neoplasms= in the brain may be the occasion of

the rupture of the vascular walls and apoplexy. =Hæmatoma= of the dura

in the dog (Friedberger and Fröhner), =cholesteatomata= in the horse,

and =carcinoma= may be apparent causes.

The effect of =mechanical injury= must be admitted, as blows on the

head, injuries from an ox yoke, and concussions during the battles of

rams and bulls.

_Lesions._ Blood extravasations may be found at any part of the brain:

a. into the brain substance; b. into the ventricles; c. from the pia

mater; d. into the arachnoid sac; e. between the skull and dura mater.

It is especially common in connection with the ganglia adjoining the

ventricles; the corpus striatum, optic thalamus, the corpora

quadrigemini, the fornix. In other cases the crus cerebri, pons, medulla

oblongata, corpus calosum. In other cases the convolutions of the

cerebrum or cerebellum suffer. The amount of effusion may be limited to

a few drops or it may cover an extensive area and cause considerable

flattening of the brain substance.

When capillary hæmorrhages are present—the size of a millet seed or a

pea—Friedberger and Fröhner have usually found them multiple, but when

large enough to form distinct clots they are usually single and confined

to one side. If a clot, involving the brain substance, is small, it

merely separates the nervous fibres, but if larger, the cerebral tissue

is broken down in the mass of clot, discolored, torn and softened. If

the patient has survived the first attack the clot passes through the

different stages of discoloration, brown, brownish yellow, yellow, and

may become fibrous forming a distinct cicatrix, with loss of brain

substance. In connection with the partial absorption of the effused

blood, cavities may be filled with a serous fluid (apoplectic cysts),

and these may show multiple loculi. The nerve fibres which lead to an

old standing lesion are usually degenerated.

When effused into a ventricle, blood is less readily absorbed and tends

to remain as a flattened discolored layer.

Extravasation between the dura mater and the cranium is probably always

the result of direct mechanical violence.

_Symptoms._ Premonitory indications of apoplexy are less commonly

recognized in the lower animals than in man, doubtless largely because

of the impossibility of appreciating subjective symptoms. The first

observed indications are usually dullness, some lack of coördination of

movement, swaying, unsteady gait, trembling and a tendency to deviate to

one side or to move in a circle. In the majority of cases, however, the

first symptoms noticed are a complete loss of consciousness or nearly

so, a sudden fall and often more or less convulsive movements of the

limbs aggravated by any excitement. The eyes remain dilated, the pupils

enlarged or sometimes contracted, and in case of unilateral effusion the

axis of vision of both eyes is turned to the affected side, right or

left. The pupil of one eye is likely to be more widely dilated than that

of the other. Rolling of the eyeballs is not uncommon. Convulsions may

occur, the head and hind limbs being drawn back forcibly as in

oposthotonos, or the animal may lie flaccid and comatose from the first.

The nasal, buccal and orbital mucous membranes are usually congested,

deep red or livid, yet sometimes they are anæmic and pale (Shock). The

breathing is usually characteristic, being deep, slow, labored,

irregular and stertorous and accompanied by puffing out of the cheeks at

each expiration (except in solipeds). Yet there are cases in which

stertor is absent. The pulse is usually slow, full and soft, and, in the

carotids, throbbing, but it may be weak and imperceptible. There may be

complete unconsciousness, and again from the first, or nearly so, there

may be a slight response to a stimulus, which cannot be referred

altogether to reflex action. In vomiting animals, emesis may ensue.

Stupor and coma are more or less marked, though liable to intermissions

under any cause of irritation.

Along with the above symptoms the spasms and sequent paralysis, are

significant. If confined to given muscles or groups of muscles

(monoplegia) it usually implies pressure on some special cortical

convolutions presiding over these muscles, and convulsions are to be

expected. If there is hemiplegia it is suggestive of implication of the

medulla or pons on the opposite side, or of a clot on the corpus

striatum or extensively on one side of the cerebrum. A clot in the

lateral ventricle tends to profound coma. So liable, however, is

pressure to be extended from one side of the brain to the other, and

irritation on the one side to rouse a corresponding condition on the

opposite side, or in related ganglia, that deductions of this kind

cannot always be implicitly relied on.

Though an animal should recover from an attack there is liable to remain

some modification of the nervous functions, partial anæsthesia,

circumscribed paresis, dullness, lack of energy, irritability, or

muscular atrophy.

Cerebral embolism and thrombosis and their sequelæ, infarction and

softening, give rise to corresponding symptoms, according to the seat of

the lesion, and like lesions of the blood vessels predispose to

subsequent attacks.

_Diagnosis_ is based largely on the appearance, usually sudden but

sometimes slow, of a more or less profound unconsciousness, attended or

followed by paralytic troubles. The history of the case may assist, any

blow on the head, or sustained by falling, striking a wall or post, or

wearing a yoke, is to be noted. Any extraordinary exertion or excitement

must be considered. Any sign of injury about the head; the congestion of

the cephalic mucous membranes in contrast with the pallor of _shock_;

the onset of the attack without convulsions (or with them as in

epilepsy); the deep coma indicating cerebral hæmorrhage or narcotic

poisoning; the absence of the odor of alcohol, opium, or other narcotic

from the breath; the turning of the eyes to one side and the inequality

of the pupils on the two sides; the turning of the head to the same side

as the eyes; the slow, labored, usually stertorous breathing; the slow,

full, soft pulse; the occasionally rigid condition of the muscles and

finally the paralysis, hemiplegic, and less frequently monoplegic or

paraplegic, make up the diagnostic picture.

_Uræmia_ and _diabetic coma_ may be excluded by examination of the

urine, _pulmonary apoplexy_ or _œdema_ by the predominance of

respiratory troubles, and fulminant _anthrax_ by the examination of the

blood and by the fact that this disease does not prevail in the

locality.

_Treatment_ is very unsatisfactory in the lower animals, as the disease

is very fatal, and unless recoveries are complete, they are not

pecuniarily desirable. It is only in the slighter cases, therefore, that

treatment can be recommended. At the very outset nothing is better than

a full bleeding in a large stream from the jugular vein or temporal

artery. Ice, snow, or cold water should meanwhile be applied to the

cranial region. Absolute rest should be given, any harness that would

impede circulation or respiration removed, and hot water or stimulating

embrocations applied to the limbs.

When consciousness returns and the patient can swallow, an active

purgative may be administered, or barium chloride or eserine may be

given subcutem. Any recurring heat of the head may be met by renewal of

cold applications, and the force of the circulation may be kept in check

by small doses of bromides or aconite. In case of the formation of a

clot, iodide of potassium and other alkaline agents may be resorted to.

Quiet and the avoidance of all excitement together with a laxative

non-stimulating diet must be secured throughout. A course of vegetable

or mineral tonics and an occasional blister to the side of the neck may

prove a useful sequel.

CEREBRAL HYPERÆMIA.

MENINGO—ENCEPHALIC CONGESTION.

Passive and active hyperæmia. Causes: _passive_: obstacles to return

of blood: anæmia: _active_: brain excitement, sun-stroke, violent

exertion, fear, abdominal tympany, ptomaines, narcotics, lead, darnel,

millet, leguminous seeds partly ripened, tumors, parasites. Symptoms:

_horse_: variable, vertigo, stupor, convulsions, apoplexy,

irritability, disorderly movements, strong, hard pulse, congested

mucosæ, heat of head, dulness, drowsiness, lethargy, coma, alternating

periods of violence, aggravated by what tends to increase vascularity

of brain, congested optic disc: _cattle_: parallel, with special heat

of horns: _dogs_: similar, with desire to move, or wander, or has

nausea, howls, snaps. Treatment: cold to head, derivation to limbs and

bowels, chloral, bromides, ergot, bleeding, darkness, coolness,

non-stimulating food.

Congestion of the encephalon is treated here as a pathological entity,

though it cannot always be distinguished clinically from some forms of

vertigo on the one hand and from the milder types of apoplexy or

encephalitis on the other. It has been divided into _passive_ or _venous

hyperæmia_ and _active_ or _arterial hyperæmia_.

_Passive hyperæmia_, as shown under vertigo and apoplexy is a common

result of a tight collar, a tight strap used for cribbiting, a too short

bearing rein, dilation or valvular disease of the right heart, or

disease of the lungs, violent efforts in running, draught, etc. It tends

to be associated with arterial anæmia on the principle that the closed

cranial cavity can only admit a certain amount of blood and if an excess

accumulates in the veins and capillaries, this must be compensated first

by the movement backward to the spinal canal of the cerebro-spinal

fluid, and second by the diminution of the blood in the cerebral

arteries.

_Active hyperæmia_ may be brought about by any excitement which

especially affects the brain. This has been already noted in connection

with insolation (sun-stroke). It may result from severe exertion during

hot weather, in a violently contested race, in drawing a heavy load up

hill, or in harsh training. Violent exertion just after a meal is

especially injurious. Also the excitement of travelling by rail, or that

caused by proximity to locomotives, to discharges of firearms and to

other causes of great fear; encreased blood tension in the cerebral

vessels in connection with hypertrophy of the left ventricle, or

obstruction in other vessels (of the limbs) so as to direct the force of

the current into the carotids, the expulsion of blood from the

splanchnic cavities by gastric or intestinal tympany, or overloading of

the paunch, and irritation of the brain by ptomaines and toxins in

certain infectious diseases (rabies, canine distemper, etc.). In the

same way vegetable narcotics (opium, etc.) produce congestion. Among the

most common causes of congestion are lead, poisoning by lolium

temulentum, partially ripened lolium perenne, millet, Hungarian grass,

and partially ripened seeds of the leguminosæ (chick vetch, vicia

sativa.). Other causes are the presence of tumors (cholesteatoma) and

parasites (cœnurus, cysticercus) in the brain.

_Symptoms._ Cerebral hyperæmia, like other brain disorders may give rise

to a great variety of symptoms, according to the condition of the animal

and the susceptibility of its nerve centres. Some cases have the

characteristic seizures of vertigo, others the manifestations of heat

stroke, and others, epileptic explosions or apoplectic symptoms. For

these see under their respective headings. In other cases the symptoms

are those of encephalo-meningitis but moderate in its type and often

tending to a transient duration, or to prompt resolution and recovery.

=Horse.= There is manifest change of the nervous and intellectual

conditions, which may show itself by irritability or restlessness, by

pushing against the wall, by hanging back on the halter, by trembling,

shaking the head, neighing, pawing and, in exceptional cases, by

rearing, biting or kicking. The pulse is hard and full, the heart’s

impulse strong, the beats in the carotids and temporal arteries being

especially forcible, and the buccal, nasal and orbital mucosæ are

strongly congested. Heat of the head is usually a marked feature. While

usually very sensitive to touch, noise or light, the animal may be dull

or drowsy, and in spite of its marked sensitiveness, it is then inert or

lethargic and indisposed to any active exertion. Freidberger and Fröhner

say that the habitual comatose condition alternates at intervals with

periods of violent excitement during which the animal pushes or dashes

against the wall, grinds the teeth, rears, paws, kicks, bites, etc., and

then relapses into the state of coma. When the disease reaches this

stage it may be questioned whether we are not dealing rather with acute

encephalitis.

In active congestion the symptoms are always aggravated by whatever

tends to increase the vascular tension in the brain. Active exertion,

draught, the pendent position of the head, the recumbent position on the

side with the head as low as the body or lower, aggravate all the

phenomena and render the animal more helpless.

The following table slightly modified from Spitzka serves to point out

the distinctions between anæmia and hyperæmia:

─────────────────┬─────────────────┬─────────────────┐

Symptoms. │ In Cerebral │ In Cerebral │

│ Anæmia. │ Hyperæmia. │

─────────────────┼─────────────────┼─────────────────┤

│ │ │

Pupils. │Usually dilated │Usually small or │

│ and mobile. │ medium. │

Respiration. │Often interrupted│Normal or nearly │

│ by a deep │ so. │

│ breath or sigh,│ │

│ even when at │ │

│ rest. │ │

Activity. │Lassitude. │Restless, but │

│ │ indisposed to │

│ │ exertion. │

Temperament. │Lethargic with │Irritable with │

│ exceptions. │ exceptions. │

Intelligence. │Senses impaired. │Impaired. │

Elevation of │Aggravates │No effect, or │

head. │ symptoms. │ improvement. │

Recumbent, │Amelioration. │Aggravation. │

dependent head.│ │ │

Straining. │Not necessarily │Aggravated. │

│ aggravated. │ │

─────────────────┴─────────────────┴─────────────────┘

=Cattle= show the same general congestion and heat of the head, ears and

horns, congested mucosæ, fixed eyes, and pupils, indisposition to follow

the herd, irritability, and dulness with often a disposition to lie

down. This may go on to violent bellowing, pushing against the wall,

grinding of the teeth, working of the jaws, rolling of the eyeballs, and

violent dashing in different directions regardless of obstacles.

=Dogs= show the same restlessness and excitability, congested head, eyes

and nose, frequent movement from place to place, a desire to wander off,

and it may be spasms. If there has been any gastric disturbance vomiting

usually supervenes. As in the larger animals the disease may go on to

more violent symptoms, and the animal howls, rushes in different

directions, and may snap at imaginary objects, or at any one who

interferes with him. His movements are liable to be unsteady, uncertain

and swaying.

In all cases the ophthalmoscope reveals a congestion of the optic disc.

In the different animals too, acute cerebral hyperæmia tends to merge

early into encephalitis with exudation and pressure, attended by stupor,

coma, somnolence or profound lethargy.

_Treatment._ In slight cases of cerebral hyperæmia, it may be sufficient

to apply cold to the head with a stimulating fomentation to the limbs,

and an active purgative, with chloral or bromides. Ergot in full doses

has often an excellent effect.

In the more acute types of the disease, bleeding is the first and most

efficient measure. A full abstraction from the jugular will relieve the

vascular tension and relieve the circulation on the brain. It has been

counselled to avoid this when comatose symptoms have set in, and in some

prostrate conditions a large and rapid abstraction of blood may fatally

increase the prostration. In other cases, however, the less rapid

abstraction will improve at once the intracranial circulation and

nutrition, and solicit the reabsorption of the exudate which produces

sopor and coma.

A purgative is one of the most efficient derivatives, the determination

of an excess of blood to the bowels and of an abundant serous discharge

into their interior acting as a valuable depletion, and abstraction of

blood from the over-excited brain. At least a half more than the usual

dose must be given, and may be supplemented by an injection of glycerine

or a hypodermic exhibition of eserine. It is best to avoid too drastic

or irritant purgatives as the cerebral congestion may be aggravated by

the irritation, as it often is induced in severe indigestions. For the

horse, aloes and podophyllin, or for ruminants, omnivora and carnivora

castor oil may be resorted to.

The patient must be placed by himself in a dark, cool, well aired

building, and when able to resume feeding must receive an easily

digested, non-stimulating diet; for horses or cattle gruels, wheat bran

mashes, pulped roots, or green food; for dogs and pigs, gruels, mush or

milk.

Any sequent paralysis must be treated on general principles.

Text book of veterinary medicine, Volume 3 (of 5) · 第 26 / 294 题