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NEUROGENIC SHOCK RESULT OF IMBALANCE BETWEEN PARASYMPATHETIC AND SYMATHETIC STIMULATION OF VASCULAR SMOOTH MUSCLE.

. IF PARASYMPATHETIC OVERSTIMULATION OR SYMPATHETIC UNDERSTIMULATION PERISISTS SUSTAINED VASODILATION OCCURS AND BLOOD POOLS IN THE VENOUS OR CAPILLARY BEDS NEUROGENIC SHOCK CAUSES DRAMATIC REDUCTION IN SYSTEMIC VASCULAR RESISTANCE AS SIZE OF THE VASCULAR COMPARTMENT INCREASES AS SYSTEMIC VASCULAR RESISTANCE DECREASES PRESSURE IN THE BLOOD VESSEL BECOMES TOO LOW TO DRIVE NUTRIENTS ACROSS THE CAPILLARY MEMBRANES AND CELLULAR METABOLISM IS IMAPIRED CONDITIONS THAT CAUSE NEUROGENIC SHOCK INCREASING PARASYMPATHETIC STIMULATION OR INHIBITING SYMPATHETIC STIMULATION OF SMOOTH MUSCLE OF BLOOD VESSELS: HEAD INJURY TRAUMA TO SPINAL CORD SPINAL SHOCK INSULIN REACTIONS HYPOGLYCEMIA DECREASING GLUCOSE TO MEDULLA CNS DEPRESSANT DRUGS SEDATIVES, BARBITUATES, NARCOTICS ANESTHESIA SEVERE PAIN PROLONGED EXPOSURE TO HEAT BRADYCARDIA OCCURS EARLY BUT TACYCARDIA BEGINS AS COMPENSATORY MECHANISMS ARE INITIATED. CENTRAL VENOUS PRESSURE DROPS AS VEINS DILATE VENOUS RETURN TO THE HEART DECREASES STROKE VOLUME DECREASES MAP FALLS (THUS BP FALLS) IN EARLY STAGES EXTREMITIES ARE WARM AND PINK FROM THE POOLING OF THE BLOOD

AS NEUROGENIC SHOCK PROGRESSES SKIN BECOMES PALE AND COOL MANIFESTATIONS OF NEUROGENIC SHOCK BLOOD PRESSURE: HYPOTENSION; PULSE: SLOW AND BOUNDING; BRADYCARDIA SKIN: WARM AND DRY MENTAL STATUS: ANXIOUS, RESTLESS, LETHARGIC PROGRESSING TO COMATOSE URINE OUTPUT: OLIGURIA TO ANURIA LOWERED BODY TEMPERATURE SPINAL SHOCK TEMPORARY LOSS OF REFLEX FUNCTION AREFLEXIA BELOW THE LEVEL OF INJURY. RESPONSE BEGINS IMMEDIATELY AFTER COMPLETE TRANSECTION OF SPINAL CORD WHEN CONNECTIONS BETWEEN BRAIN AND SPINAL CORD ARE INTERRUPTED AND CORD DOES NOT FUNCTIONAL AT ALL. SPINAL SHOCK ALSO OCCURS TO VARYING DEGREES AFTER PARTIAL TRANSECTION AS WELL AFTER SPINAL CORD CONTUSIONS, COMPRESSION, AND ISCHEMIA WHEN DAMAGE FROM INJURY STOPS IMPULSES FROM THE BRAIN SPINAL SHOCK FOLLOWS. LOSS OF MOTOR FUNCTION LOSS OF TENDON REFLEXES LOSS OF AUTONOMIC FUNCTION SPINAL SHOCK MAY BEGIN WITHIN 1 HOUR FROM INJURY USUALLY LASTS 2 WEEKS (BOOK SAYS 1 TO 6 WEEKS, INSTRUCTOR SAYS 2 WEEKS) SPINAL SHOCK ENDS SLOWLY GRADUAL REAPPERANCE OF RELFEXES, HYPERREFLEXIA INCREASED REFLEXES, MUSCLE SPASTICITY, AND REFLEX BLADDER EMPTYING. MANIFESTATIONS OF ACUTE SPINAL SHOCK FLACCID PARALYSIS OF SKELETAL MUSCLE BELOW THE LEVEL OF INJURY

LOSS OF ALL SPINAL REFLEXES BELOW THE LEVEL OF INJURY LOSS OF SENSATIONS OF PAIN, TOUCH, TEMPERATURE, PRESSURE, BELOW LEVEL OF INJURY ABSENCE OF VISCERAL AND SOMATIC SENSATIONS BELOW LEVEL OF INJURY BOWEL AND BLADDER DYSFUNCTION LOSS OF ABILITY TO PERSPIRE BELOW THE LEVEL OF INJURY

PERSON WITH CERVICAL OR UPPER THORACIC SCI MAY ALSO HAVE NEUROGENIC SHOCK RESULTING IN CARDIOVASCULAR CHANGES THESE CHANGES ARE DUE TO THE INABILITY OF HIGHER CENTERS IN THE BRAINSTEM TO MODULATE REFLEXES. AS A RESULT VASCULAR BEDS BELOW THE LEVEL OF INJURY DILATE CARDIAC ACCELERATOR RELFEX IS SUPPRESSED BRADYCARDIA PATIENT EXPERCIENCES HYPOTENSION BRADYCARDIA OTHER MANIFESTATIONS **MAY** INCLUDE o RESPIRATORY INSUFFIENCY DUE TO LOSS OF INTERVENTION OF DIAPHRAGM AT C1 TO C4 INJURIES o HYPOTHERMIA o PARALYTIC ILEUS o URINARY RETENTION o OLIGURIA o BOTH BRADYCARDIA AND HYPOTENSION MAY PERISIST EVEN AFTER SPINAL SHOCK RESOLVES IN ADDITION LOSEING SYMPATHETIC CONTROL OF HEART RATE THE CLIENT WITH HIGH LEVEL SCI EXPERINCES DECREASED PERIPHERAL RESISTANCE AND LOSS OF MUSCLE ACTIVITY THESE CHANGES RESULT IN SLUGGISH BLOOD FLOW AND DECREASED VENOUS RETURN INCREASED RISK FOR THROMBOPHLEBITIS DVT UPPER MOTOR NEURON LESIONS

UPPER MOTOR NEURONS CEREBRAL CORTEX THALAMUS BRAINSTEM CORTICOSPINAL TRACT CORTICOBULBUR TRACTS RESPONSIBLE FOR VOLUNTARY MOVEMENTS WHEN THESE MOTOR PATHWAYS ARE INTERRUPTED THE CLIENT EXPERIENCES SPASTIC PARALYSIS AND HYPERREFLEXIA AND MAY BE UNABLE TO CARRY OUT SKILLED MOVEMENT PATIENT WILL EXPERIENCE SPINAL SHOCK AND FLACCID PARALYSIS PRIOR TO SPASTIC PARALYSIS, THE SPINAL SHOCK WILL RESOLVE AND FLACCID PARALYSIS AS WELL BUT SPASTIC PARALYSIS WILL NOT

LOWER MOTOR NEURONS LOCATED IN THE ANTERIOR HORN OF THE SPINAL CORD THE MOTOR NUCLEI OF BRAINSTEM AND THE AXONS THAT REACH THE MOTOR END PLATE OF SKELETAL MUSCLES RESPONSIBLE FOR THE INNERVATION AND CONTRACTION OF SKELETAL MUSCLES INTERRUPTION OF LOWER MOTOR NEURONS RESULT IN FLACCIDITY AND EXTENSIVE MUSCLE ATROPHY WITH LOSS OF BOTH VOLUNTARY AND INVOLUNTARY MOVEMENT IF ONLY SOME OF THE MOTOR NEURONS SUPPLYING THE MUSCLES CLIENT EXPERIENCES PARTIAL PARALYSIS PARESIS IF ALL MOTOR NEURONS TO MUSCLE ARE AFFECTED COMPLETE PARALYSIS WITH HYPOREFLEXIA

PARAPLEGIA THORACIC, LUMBAR, SACRAL PORTIONS OF SPINAL CORD ARE INJURED CAUSING LOSS OR IMPAIRMENT OF SENSORY AND/OR MOTOR FUNCTION LOWER PORTION OF BODY, SOMETIMES LOWER TRUNK QUADRIPLEGIA CERVICAL SEGMENTS OF CORD ARE INJURED IMPAIRING FUCNTIONS OF ARMS, TRUNK, LEGS, PELVIC ORGANS AUTONOMIC DYSREFLEXIA = AUTONOMIC HYPEREFLEXIA NOT SPINAL SHOCK SEEN ONLY AFTER RECOVERY OF SPINAL SHOCK EXAGERRATED SYMPATHETIC RESPONSE THAT OCCURS CLIENTS WITH SCIs AT OR ABOVE T6 LEVEL WITH THIS RESPONSE SEEN AFTER RECOVERY OF SPINAL SHOCK OCCURS AS RESULT OF A LACK OF CONTROL OF THE AUTONOMIC NERVOUS SYSTEM BY HIGHER BRAIN CENTERS WHEN ANY SENSORY STIMULI ARE UNABLE TO ASCEND TO CORD, MASS REFLEX STIMULATION OF SYMPATHETIC NERVES BELOW THE LEVEL OF INJURY CORD AREA OCCURS TRIGGERING MASSIVE VASOCONSTRICTION IN RESPONSE THE VAGUS NERVE CAUSES BRADYCARDIA WITH HYPERTENSION, AND VASODILATION ABOVE THE LEVEL OF THE INJURY IF UNTREATED AUTONOMIC DYSREFLEXIA CAN CAUSE SEIZURES STROKE MYOCARDIAL INFARCTION POTENTIALLY FAILURE DUE TO MASS REFLEX FROM STIMULATION OF SYMPATHETIC NERVES BELOW THE LEVEL SCI AUTONOMIC DYSREFLEXIA TRIGGERED BY STIMULI THAT WOULD NORMALLY CAUSE ABDOMINAL DISCOMFORT 1. FULL BLADDER MOST COMMON CAUSE 2. BY STIMULATION OF PAIN RECEPTORS 3. BY VISCERAL CONTRACTIONS CAUSES OF AUTONOMIC DYSREFLEXIA INCLUDE

FECAL IMPACTION BLADDER INFECTIONS AND STONES INTRAUTERINE CONTRACTIONS EJACULATIONS PERITONITIS STIMULATION FROM PRESSURE ULCERS INGROWN TOENAILS MOST COMMON PRECIPITATING EVENT IS BLOCKED URINARY CATHETER MANIFESTATIONS OF AUTONOMIC DYSREFLEXIA MASSIVE REFLEX STIMULATION OF SYMPATHETIC NERVES BELOW THE LEVEL OF SCI, TRIGGERING MASSIVE VASOCONSTRICTION; RESPONSE IS VAGUUS NERVE CAUSE BRADYCARDIA AND VASODILATION ABOVE SCI POUNDING HEADACHE (VAGAL STIM) VASODILATION ABOVE SCI) BRADYCARDIA VAGAL STIMULATION HYPERTENSION HIGH BP IP TP 300/160 REFLEX SYMPATHETIC RESPONSE FLUSHED WARM SKIN WITH PROFUSE SWEATING ABOVE THE LESION PALE, COLD, DRY SKIN BELOW SCI LESION ANXIETY AUTONOMIC DYSREFLEXIA IS A MEDICAL EMERGENCY
Autonomic dysreflexia occurs when there is an unrelieved stimulation of sensory receptors below the level of the cord lesion. Frequently seen within the first year following a spinal cord injury at T6 or above. The disconnection of the spinal sympathetic centres from supraspinal control causes the predisposition to autonomic dysreflexia. The intact autonomic nervous system reacts to this stimulus by releasing catecholamines. This induces vasoconstriction of the blood vessels above the level of injury, and produces a reflex arteriolar spasm that increases the blood pressure, resulting in hypertension. Baroreceptors in cerebral vessels, carotid sinus and aorta detect the hypertension and stimulate the parasympathetic nervous system by sending an inhibitor signal to the medulla. Due to the spinal cord injury, this message cannot transverse the cord and therefore vasoconstriction occurs above the cord lesion, causing headaches, flushing and nasal congestion, whereas vasodilatation is evident below the lesion.

The heart rate is slowed via the vagus nerve in an attempt to control the rise in blood pressure. However, the visceral and peripheral vessels are unable to dilate because the efferent impulses are unable to pass through the cord lesion. This results in the characteristic hypertension and bradycardia. Any noxious stimuli below the level of injury can trigger autonomic dysreflexia. The first steps should involve locating the stimulus and removing it. This should be done in conjunction with efforts to control the increasing hypertension. It should be noted that the increase in arterial pressure could be so acute that it may induce a cerebral vascular accident or myocardial infarction. IT is important to remember that many individuals with lesions of T6 or above may have a lower than normal blood pressure, so a blood pressure of 120/80 may represent a substantial rise. When trying to locate the noxious stimulus it should be remembered that anything could potentially induce this reaction including pregnancy, erections, drugs and many other stimuli. The bladder and bowels should be checked initially as these are the most common causes. If a patient has a urinary catheter it may be kinked or blocked. Loosen all clothing, check skin for pressure sores and check for toe damage and remove the stimuli wherever possible. Sitting the patient up may induce orthostatic hypotension and may assist in counteracting hypertension; however, if this proves to difficult or unsafe then the administration of one of the following drugs to relieve the hypertension: - Phentolamine 5-10mg intravenously - Gylceryl trinitrate 300 micrograms sublingually or - Nifedipine 5-10mg sublingually. Irrigation of a catheter should be done slowly and gently (Ahrens and Prentice, 1998) to reduce the risk of sudden hypotension or inducing bladder spasms, which may aggravate the current situation. A digital rectal examination should be conducted following the application of a local anaesthetic to reduce rectal stimulation and to prevent an increase in the current symptoms. If it is thought that the onset is due to constipation/the need to defecate, then the stool should be removed gently and gradually. If symptoms persist or worsen the procedure should be stopped. If symptoms subside then the process can continue cautiously

EMERGENCY CARE OF SCI

C1-C4 LEVEL RESPIRATORY PARALYSIS IS COMMON REQUIRES VENTILATOR ASSISTANCE TO BREATHE BELOW C4 INCREASED RISK OF RESPIRATORY FAILURE AND MAY REQUIRE INTUBATION IF EDEMA ASCENDS THE CORD PREHOSPITAL MANAGEMENT INCLUDES RAPID ASSESSMENT ABCs AIRWAY BREATHING CIRCULATION, IMMOBILIZATION STABALIZING THE HEAD AND NECKOARD AVOID FLEXING, EXTENDING OR ROTATING NECK MAINTAIN PATIENT IN SUPINE POSITION DO NOT PUT PATIENT IN SHOCK POSITION TRANSFER USING BACKBOARD RESPIRATORY DISTRESS IN CLIENT WITH CERVICAL LEVEL INJURY IS TREATED BY PLACING PATIENT ON VENTILATOR OXYGEN IS ADMINSTERED TO CLIENT WITH THORACIC LEVEL INJURY PARALYTIC ILEUS IS COMMON IN PATIENTS WITH SCI AND IS TREATED BY THE INSERTION OF NG TUBE WITH CONNECTION TO SUCTION TO PREVENT OVERDISTENSION OF ATONIC BLADDER INDWELLING CATHETER IS INSERTED AND CONNECTED TO DEPENDENT DRAINAGE CARDIOVASCULAR STATUS IS ASSESSED CONTINOUSLY BY INSERTING INVASIVE MONITORING DEVICES SWAN-GANZ CARDIAC MONITOR ARTIAL MONITORING IDENTIFY HYPOTENSION AND DRAW ABGs HIGH DOSE STERIOD PROTOCOL USING METHYLPREDNISOLONE (MEDROL) WITHIN 8 HOURS OF INJURY TO IMPROVE NEUROLOGIC RECOVERY, REDUCE SPINAL SHOCK. PREVENT SECONDARY SPINAL CORD INJURY FROM EDEMA AND ISCHEMIA DIAGNOSIS

XRAY OF SPINE CT SCAN MRI OF SPINE ABGs DETERMINE RESPIRATORY INSUFFICIENCY CAN INDICATE IF DIAPHRAGM IS WEAK

MEDICATIONS NEUROGENIC SHOCK AND SPINAL SHOCK


GOAL DECREASING EDEMA FROM INJURY, TREATING HYPOTENSION AND BRADYCARDIA FROM SPINAL SHOCK, TREATING SPASTICITY 1. CORTICOSTEROIDS DECREASE/CONTROL EDEMA OF SPINAL CORD 2. VASOPRESSORS IN IMMEDIATE ACUTE CARE STAGE TO TREAT BRADYCARDIA OR HYPOTENSION DUE TO SPINAL AND NEUROGENIC SHOCK a. DOPAMINE = INOTROPIN INCREASE CARDIAC OUTPUT + HYPOTENSION IN NEUROGENIC SHOCK b. DOBUTAMINE = DOBUTREX INCREASE CARDIAC OUTPUT + SUPPORT CARDIAC FUNCTION c. ATROPINE AT BEDSIDE FOR TX OF BRADYCARDIA 3. ANTISPASMOTICS 4. ANALGESICS 5. PROTON PUMP INHIBITORS PREVENT STRESS INDUCED GASTRIC ULCERS 6. ANTICOAGULANTS HEPARIN/WARFARIN PREVENT THROMBOPHLEBITIS 7. STOOL SOFTENERS FOR BOWEL TRAINING

ASSESSMENT FINDINGS 1. CERVICAL INJURY a. Paralysis or weakness of extremities b. Respiratory distress manifested by changes in ABG studies, cyanosis, flaring of nostrils, use of accessory muscles in respiration, and restlessness c. Pulse rate below 60bpm d. Systolic BP < 80 e. Decreased peristalsis f. Requires intubation and mechanical ventilation 2. THORACIC AND LUMBAR INJURY a. PARALYSIS AND WEAKNESS OF EXTREMITIES

3. SPINAL SHOCK a. LOSS OF SKIN SENSATION b. FLACCID PARALYSIS AREFLEXIA c. ABSENT BOWEL SOUNDS d. BLADDER DISTENSION e. DECREASING BLOOD PRESSURE f. ABSENCE OF CREMASTERIC RELFEX IN MALES RETRACTION OF LEFT OR RIGHT TESTICLE IN RESPONSE TO STIMULATION OF SKIN OR RESPECTIVELY THE INNER LEFT OR RIGHT THIGH Neurogenic shock is a distributive type of shock resulting in hypotension, occasionally with bradycardia that is attributed to the disruption of the autonomic pathways within the spinal cord. Hypotension occurs due to decreased systemic vascular resistance resulting in pooling of blood within the extremities lacking sympathetic tone. Bradycardia results from unopposed vagal activity and has been found to be exacerbated by hypoxia and endobronchial suction. Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated. It is not to be confused with spinal shock, which is not circulatory in nature. The trauma causes a sudden loss of background sympathetic stimulation to the blood vessels. This causes them to relax (vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance). Treatment Fluid is always the initial treatment of shock, especially since concomitant hemorrhagic shock must be excluded following trauma. Most institutions will additionally utilize pressor agents to achieve hemodynamic stability. Dopamine (Intropin) is often used either alone or in combination with other inotropic agents. Vasopressin (antidiuretic hormone [ADH]) Certain vasopressors (ephedrine, norepinephrine). Phenylephrine may be used as a first line treatment, or secondarily in patients who do not respond adequately to dopamine.

Atropine (administer if bradycardia is severe.) Neurogenic Shock* *Hemodynamic phenomenon* Loss of vasomotor tone & Loss of sympathetic nervous system tone > inpaired cellular metabolism *Critical featuresHypotension (due to massive vasodilation Bradycardia- due to unopposed parasympathetic stimulation Poikilothermia; *Unable to regulate temperatureOccurs Within 30 min cord injury level T 5 or above; last up to 6 weeks; also due to effect some drugs that effect vasomotor center of medulla as opioids, benzodiazedines Management (*Determine underlying cause) Airway support Fluids as needed- Typically 0.9 NS , rate depends upon need Atropine for bradycardia Vasopressors as phenylelphrine (Neo-synephrine) for BP support Spinal Shock *Due to acute spinal cord injury *Absence all voluntary and reflex neurologic activity below level of injury Decreased reflexes Loss of sensation Flaccid paralysis below injury Lasts days to 2 weeks (Transient) *Spinal shock & neurogenic shock can in same patient-BUT not same disorder (some sources may group both together)