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Certified Emergency Nurse (CEN) Exam Review Jeff Solheim NEUROLOGICAL EMERGENCIES Objectives: At the completion of this section, the learner will be able to: Differentiate between early and late signs of increased intracranial p ressure Discuss care of the patient with a basilar sku ll fracture Define autonomic dysreflexia Recognize medicat ions used in the treatment of seizu res Verbalize d ischarge instructions that should be provided to patients with Myasthenia Grav is The CEN exam contains fifteen questions on neurological emergencies which i nvol ve the followi ng topics: Alzheimer’s Disease/Dementia Chronic Neurological Disorders (e.g. Multip le Sclerosis, Myasthenia Grav is) Gu illain-Barre Syndrome Headache (including temporal arteritis, migraine) Increased intracranial pressure Meningitis Seizure d isorders Shunt Dysfunctions Spinal cord in juries Stroke (e.g. Ischemic or hemorrhagic) Transient Ischemic attack (TIA) Trau ma Increased intracranial pressure (ICP) Cran ial Vau lt consists of three constituents: brain, cerebral spinal fluid (CSF) and blood. Normal ICP: 0 - 15 mm Hg Elevated ICP: > 20 mm Hg Extremely high ICP may lead to herniation of the brain. Clin ical Manifestations of increased intracranial p ressure: Level of Consciousness Pupils Motor Function Vital Signs EARLY S IGNS (Increased ICP) More stimu lation required to get same response Sluggish response to light Loss of one or mo re grades on the strength scale Tachycardia, hypertensive swings LATE S IGNS (Herniation) Arousable only with deep pain or unarousable Fixed or d ilated Posturing or no response Cushing’s response Definiti on: Cushing’s Triad – Abnormal set of vital signs often associated with advanced or increased intracranial pressure. Includes: Profound bradycardia Abnormal respirations Increased systolic pressure (widened pulse pressure) Treat ment Reduce ICP by reducing the constituents of the skull: Brain Diuret ics Hypertonic solutions Blood Patient position Maintain normothermia Prevent/ treat seizures Reduce noxious stimuli Suctioning CSF Flui d Surgical decompression CSF drainage catheter 1 |P age Certified Emergency Nurse (CEN) Exam Review Jeff Solheim Shunt Dysfunction Problem Sympto ms Obstructed shunt Infected shunt Overdrainage o Signs of ICP (irritability, headache, neck pain, vo miting, bulg ing fontanels, new seizures, change in behavior.) Signs of obstruction Local wound problems Unexplained fevers Redness, edema and tenderness along skin over the shunt. Signs of peritonitis (if shunt terminates in the abdomen.) Depressed fontanels Overlapping of sku ll bones headache when upright, when supine Subdural hemato mas Treat ment As per ICP for head injury Flushing of the shunt. Antibiotics Sepsis protocols Replacement of shunt Supportive therapy (oxygen, treat seizures and bleeds as per protocols. Suction PRN Glasgow Co ma Scale Best Motor Response Obeys simple co mmands Localizes noxious stimulus 6 5 Flexion withdrawal 4 Abnormal flexion Abnormal extension No motor response 3 2 1 Best Verbal Response Oriented Confused Verbalizes, inappropriate words Vocalizes – moans/groans No verbal response 5 4 Eye Opening Spontaneously To speech 4 3 3 To noxious stimulus 2 2 1 No eye opening 1 Eyes and pupils Size – pupils should be with in 1 mm in size o f one another. Anisocoria: pupils that are more Shape – pupils are normally round. Irregularly shaped pupils, especially oval, than one millimeter different in size. indicate dysfunction or pressure on oculomotor nerve III. Anisocoria occurs normally in as many as 20 – 25% of patients, and Degree of reactivity – both pupils should rapidly constrict when light is shone is more co mmon with age. into one of them. Best motor response Assess motor and sensory function or weakness, loss of movement or altered sensation to any part of the body Assess for pronator drift in the conscious, cooperative patient: ask the patient to close his or her eyes, and extend the arms out directly in front of them, ho lding this position for 30 seconds. If one arm drifts downward ahead of the other, it is an indicator of weakness to that side of the body. Deficits fro m the neck up affect the same side as the brain lesion (ipsilateral) and deficits fro m the neck down affect the opposite side as the brain lesion (contralateral) - paresis (such as hemiparesis) indicates weakness to an area of the body. -plegia (such as paraplegia) indicates paralysis to an area of the body. 2 |P age Certified Emergency Nurse (CEN) Exam Review Reflex Corneal reflex Gag reflex Swallo wing reflex Jeff Solheim If a patient’s level of consciousness does not allow them to cooperate with assessments, apply painful stimuli and look for the patient’s reaction. The fo llo wing are listed in order fro m most favorable response to least favo rable response in terms of outcome: Localizing pain – reaching toward the painfu l stimulus Withdrawal – mov ing the extremity away fro m the painfu l stimulus Decorticate posturing – abnormal flexion posture: the arms, wrists, and fingers are flexed, the arms are adducted, while the legs are fu lly Memory Tip – Decort icate has the word “core” in it and patients maintain a extended and internally rotated with plantar flexion o f position with their hands adducted to the the feet. core of their body. Decerebrate has Decerebrate posturing – abnormal extension posture: the mu ltip le “e’s” in it and “extension” starts arms are stiffly extended and abducted, and the hands with an “e”; Pat ients who are decerebrate are hyperpronated. The legs and feet remain unchanged extend their hands away fro m their body. fro m decorticate posturing. Flaccid – no motor response Superficial reflexes – normal when present, abnormal when absent Method of Elicitation Brush a wisp of cotton against the cornea or apply a small drop of water or saline to the cornea. Stimu late the back of the pharynx. Touch the uvula. Normal Response The eyelid closes quickly. The patient retches or gags. The uvula elevates. Pathological reflexes – abnormal when present, normal when absent. (These reflexes are normal in in fants, but disappear in toddlers.) Reflex Method of Elicitation Grasp reflex Stimu late the palm of an unresponsive patient’s hand. Babinski reflex Stroke the lateral aspect of the foot. Reflex Tests Doll’s eyes test (oculocephalic reflex) Pathol ogical (Positi ve) Res ponse The patient closes the fist and grasps. Great toe extension occurs. Move the patient’s head briskly to the right or left. Normal: patient’s eyes will deviate away fro m the direction the head is rotated. Abnormal: Eyes remain midline or move in a dysconjugate manner. Water Calo ric Test (oculovestibular reflex) Ice water is injected in the ear. Normal: both eyes move in the direction of the side water is instilled. Abnormal: Both eyes do NOT move in the direction of the side water is instilled. A Glasgow Co ma Score of 13 – 15 is normal or mild brain in jury, a score of 9 to 12 is moderate brain injury and a sc ore of 3 – 8 is profound brain injury. Specific Brain In juries Diffuse A xonal In jury (disruption of axons in the cerebrum which leads to a disconnection of the cortex and the brain -stem reticular formation). Clin ical Manifestations Decorticate or decerebrate posturing Loss of brain stem reflexes Hypertension Hyperthermia Excessive sweating Treat ment is to decrease ICP and support the patient. 3 |P age Certified Emergency Nurse (CEN) Exam Review Jeff Solheim Intracerebral b leeds Ep idural b leed (bleeding between the skull and the dura mater, usually from the midd le meningeal artery) Clin ical manifestations are rapid progression of increasing ICP. Memory t ip – The meninges PAD the Patients may have a period of unconsciousness follo wed by a lucid brain – the letters in PA D can be used period than begin to lose consciousness again. to help remember the order of the Often co mplain of severe headache, may have hemiparesis and dilated men inges from brain to the skull pupil on the side of the injury Pia is the innermost membrane that Subdural bleed (bleeding between the dura mater and the subarachnoid directly covers the brain. Arachnoid is the middle layer mater, usually from small bridging veins) Dura is the outermost layer closest to Clin ical manifestations will be signs of increasing ICP. the skull. Because this bleed is venous, clinical man ifestations are usually slower to manifest than with an epidural b leed. Acute Subdural bleed – sympto ms occur within 48 hours Subacute Subdural bleed – sympto ms manifest 2 – 14 days later. Chronic Subdural bleed – sympto ms take longer than 14 days to manifest Clin ical features are: Loss of consciousness Hemiparesis Fixed, dilated pupils These findings are slower onset and less severe in slow onset bleeds. Subarachnoid bleed Signs and symptoms Headache “worst headache of my life” or “thunderclap headache” Unrelieved by conventional therapies May complain of “warn ing leaks” in weeks preceding the bleed. Nausea and vomiting Photophobia Sudden seizure Meningeal signs (fever, nuchal rigidity) Treat ment Measures to reduce ICP Calciu m channel blockers Surgical intervention to control hemorrhage and manage ICP. \ Basilar Sku ll Fracture (Fracture at the base of the skull in the anterior, middle or posterior fossa) Clin ical Manifestations Anterior Fossa • • • • • • • • • Anosmia Ep istaxis Rh inorrhea Subconjunctival hemorrhage Hemorrhage in the periorb ital spaces (Raccoon’s eyes) Visual d isturbances Altered eye movement Ptosis Loss of sensation to forehead, cornea and nare Middle Fossa • • • • • • Loss of sensation to lower face Facial palsy Deafness Tinnitus Hemotympanu m Otorrhea Posterior Fossa • • Ecchy mosis behind the ear (battle sign) Impaired gag reflex 4 |P age Certified Emergency Nurse (CEN) Exam Review Jeff Solheim Definiti on – Hal o Test – Allow blood fro m the nose or ear to drop on a piece of gauze. If CSF flu id is in the blood, a yello w ring or halo will appear around the outside of the blood drop. Definiti on: Battle’s sign – bruising in the mastoid sinus, noted behind the ear. May take 24 hours post-injury to appear. Definiti on – Gl ucose test – A llo w clear drainage fro m the nose to drop on a glucose s trip. CSF flu id is high in glucose, nasal discharge is not. Definiti on: Anosmia– inability to perceive smells Definiti on: Raccoon’s sign – periorbital ecchymosis secondary to intra-orbital bleeding Treat ment Antibiotics Halo test Monitor for, and treat, increased intracranial pressure Avoid: Nose blowing Sneezing Nasal cannula Dressings Nasal intubation NG insertion Spinal cord in juries Posterior Cord transmits: Light touch Proprioception Vibrat ion Lateral Cord transmits Pain Temperature Anteri or Cord transmits: Motor function Lateral nerves cross over low where they enter the spinal cord. Anterior and posterior nerves cross over high near the base of the brain. Co mplete cord injuries Nerve Level Muscles innervated Patient Response C-4 Diaphrag m Ventilat ion C-5 Deltoid, biceps, brachioradialis Shrug shoulders, flex elbows C-6 Wrist extensor Extend wrist C-7 Triceps Extend elbow C-8 Flexo r d igitoru m profundus Flex fingers T-1 Hand intrinsic muscles Spread fingers T - 2 – L-1 Intercostals Vital Capacity L-2 Iliopsoas Hip Flexion L -3 Quadriceps Knee Extension L-4 Tibilalis anterior Ankle dorsiflexion L-5 Extension hallucis longus Ankle eversion 5 |P age Certified Emergency Nurse (CEN) Exam Review Injury Anterior Co rd Posterior Cord Central Co rd Syndrome Bro wnSèquard Cauda equina syndrome Partial cord syndromes Manifestati on Loss of motor function, loss of pain, temperature, crude touch and crude pressure. Intact proprioception, fine touch, fine pressure, and vibration Loss of proprioception, vibration, fine touch, and fine pressure Intact motor function, pain, temperature, crude touch, crude pressure Proportionally g reater loss of motor function in upper extremit ies than lower extremities with variable sensory sparing (Sensory loss is variable, more likely to lose pain and/or temperature than proprioception and/or vibration ) Loss of motor function, proprioception, and vibration sense on side of injury Loss of pain and temperature on opposite side of inju ry Caused by damage to the lower spinal cord. Results in varying degrees of motor and sensory loss in the lower body. The patient may experience problems with bowel and bladder control (especially urine retention) and sexual function. Spinal shock versus Neurogenic shock Definition Manifestations o Jeff Solheim Spinal shock Concussion to the nervous tissue of the spinal cord resulting in temporary loss of sensation and movement. – Temporary loss of: – Sensory function – Motor function – Reflexes – Bowel and bladder dysfunction Neurogenic shock Loss of sympathetic tone secondary to damage to the sympathetic fibers of the spinal cord. – Hypotension – Bradycardia – Bradypnea – Priapism – Poikilothermy Treat ment Treat neurogenic shock as per shock lesson Provide cervical stabilization of the neck and back. Manual stabilization, C-Co llars/head blocks/ back boards Maintain align ment in position found, do not force anyone with airway d ifficu lties into align ment Padding under head of child Tip backboard of pregnant patient. Autonomic Dysreflexia Sympathetic stimulat ion to lower part of body secondary to noxious stimu li (full bladder, full rectu m, acute abdomen, decubitus ulcer, renal calculi, and cystitis) results in vasoconstriction below the level of the injury, forcing blood into the upper part of the body Baroreceptors sense sudden elevation in BP and turn on parasympathetic nervous system resulting in bradycardia and vasodilation above the level of the inju ry. 6 |P age Certified Emergency Nurse (CEN) Exam Review Jeff Solheim o Clin ical Manifestations Sudden severe headache Hypertension Sweating Card iac dysrhythmias (tachycardia or bradycardia) Flushing above the level of the injury and coolness below the level of the injury Nasal stuffiness Patient may appear an xious o Treat ment Identify and rectify the cause Ganglionic Blockers such as Hydralazine (Apresoline) to reduce blood pressure Measures to reduce intracranial pressure Headaches Common Feature Length of Headache Type of Pain Location of Pain Physical Acti vity Accompanyi ng Symptoms Migraine Aura (classic) No Aura (co mmon) 4- 72 hours Severe, pulsatile, throbbing Usually unilateral Aggravated Photophobia, phonophobia, facial paleness, nausea and vomit ing Cluster Occurs in clusters, seasonal 15 to 180 minutes Excruciat ing, “suicidal” Behind one or both eyes Incapacitated Facial flushing, nasal congestion, drooping eyelid, pupillary changes o Treat ments o Migraine headache Cold packs Darkened room Pharmacology (analgesics, anti-in flammatory agents, beta-adrenergic blockers, Serotonin antagonists, Vasoconstrictors, Anti-depressants, Diuretics, Antihistamines, Steroids.) o Cluster headache – high flow o xygen Teaching Points for headache sufferers: Women should avoid oral contraceptives Avoid the following foods o Ethanol o Foods containing tyramines (beer, aged cheeses) o Caffeinated beverages o Nitrates (hot dogs, salami, processed meats, ham, bacon, yeast) o Monosodium g lutamate (packaged soups, chocolate) Seizures Seizures Seizures Generalized Tonic-Clonic •Tonic phase •Clonic phase •Post-ictal phase Absence •Ages 4 – 12 •< 15 seconds •Automatism Partial Complex Simple Unaware Aware •Involves: •Focal motor activity •Somatic sensory experiences •Disturbances in vision, hearing, smell or taste •Usually unilateral 7 |P age Certified Emergency Nurse (CEN) Exam Review Jeff Solheim Treat ment Airway Consider Dext rose 50% and rapid cooling Benzodiazep ines to stop seizures Anticonvulsants to prevent recurrence Phenytoin (Dilantin) Never give in dextrose containing solution (give in NS) Has a high pH, will cause severe local tissue necrosis in cases of infiltration (g ive antecubital or central line) Elevate limb, apply d ry heat and cool compresses after extravasation Side effects Hypotension Heart blocks Bradycardia Phenobarbital Monitor for respiratory suppression, central nervous system depression and hypotension Fosphenytoin Sodium (Cerebyx) Expensive Used for status epilepticus Monitor for Hypotension Depressed respirations Meningitis (Infection of the pia or arachnoid meninges) Causative agents Fungus – rare, associated with immu moco mpro mise Virus – mild, short lived, non-contagious with gradual onset of symptoms Bacteria - life threatening with acute onset of symptoms. Sources include blood, basilar sku ll fractures, infected facial structures, brain abscesses. Clin ical Manifestations Headache (especially occip ital) Altered mental status/malaise Hyperreflexia/seizures Nuchal rigid ity Fever and chills Signs of sepsis (tachycardia, tachypnea, hypotension) Patients with meningococcal meningit is may present with a non -blanching petechial rash on the torso and legs. Pediatric specific signs: Vo mit ing, anorexia, and poor feeding Altered mental status High-pitched cry in the infant Bulg ing of the fontanels Bradycardia Biot’s respirations Treat ment Assume it is bacterial – negative pressure room and masks Introduce measures to reduce intracranial pressure Assist with lu mbar puncture Initiate antibiot ics (may be stopped if viral) Admin ister antipyretics and analgesics Provide prophylaxis for all close contacts of bacterial men ingitis 8 |P age Certified Emergency Nurse (CEN) Exam Review Jeff Solheim Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig’s disease) (Neurodegenerative disease results in inability of the voluntary motor nerves to transmit impulses, resulting in loss of motor function and muscle degeneration.) Usually starts in one limb and is marked by twitching, cramping, and stiffness of the affected muscles. With time, the patient may beco me unstable when walking or have difficulty with fine motor control when writ ing or buttoning a shirt. Ult imately, all limbs are affected, respiratory muscles weaken, respiratory co mplications become co mmon, and the swallowing muscles may weaken, leading to choking and aspiration. The speech becomes slurred and nasal. No cure, supportive therapy only Multiple Sclerosis (MS) Autoimmune disease which comes in sporadic attacks, brought about by triggers such as viruses, pregnancy, stress, and the spring and summer seasons. An attack can cause blurred or double vision, red-green co lor distortion, blindness in one eye, weakness, and difficu lty with coordination and balance. Paresthesia, pain, speech impairment, tremors, and dizziness also may occur. The first attack typically occurs between ages 20 and 40. The symptoms of an attack may resolve completely, but if the patient has successive attacks, some sympto ms may worsen and persist. No cure exists for MS, but steroids may reduce the severity of attacks, and interferon beta (Rebif) and immunosuppressants may min imize the symptoms. Memory Tip – The sympto ms of Parkinson’s disease (Loss of dopamine producing cells in the brain) Parkinson’s disease may be Sympto ms remembered using the mnemonic Depression TRAP: Difficulty swallowing or speaking Tremo rs Urinary problems or constipation Rig idity Sleep disruptions. Akinesia and Bradykinesia Treated with drugs that replace or stimulate production of dopamine Postural instability Myasthenia Gravis (Marked by muscle weakness often exacerbated by activity) Weakness often manifested by drooping eyelids or diplopia, weakness of the throat muscles with speech alteration s and difficulty swallowing. Severe cases may depress the respiratory system or cause complete respiratory arrest. Admin istration of Edrophonium (Tensilon) improves symptoms. Controlled with medications such as such as pyridostigmine (Mestinon), barbitura tes, opiates, quinidine (Quinidex), quinine, corticotropin (Acthar), cort icosteroids, aminoglycosides, antibiotics, and muscle relaxants. Gu illain-Barre [GBS] (acute inflammatory polyneuropathy that primarily affects the motor component of the peripheral nerves) Progression of illness Mild febrile illness 2 to 3 weeks prior to onset of GBS Neuropathy begins in lower ext remities and ascends in symmetrical pattern May affect respiratory muscles and cause respiratory insufficiency. Usually peaks in one week with motor function returning in descending fashion. Treat ment Largely supportive Onset may be arrested with plasmaphoresis or administration of IV immunoglobulins. 9 |P age Certified Emergency Nurse (CEN) Exam Review Jeff Solheim Practice Questions Which of the follo wing factors would contribute to a suspicion of men ingitis? a. b. c. d. The patient’s mother had men ingitis as a child The patient is on oral antibiotics for periorb ital cellulitis The patient was out camping in the woods the weekend preceding this ED visit The patient had open heart surgery to repair a congenital heart defect at the age of five Which of the follo wing blood pressure changes is associated with increased intracranial pressure? a) b) c) d) Widening pulse pressure Decrease in systolic pressure Increase in diastolic pressure Declining mean arterial pressure A patient receiving intravenous phenytoin (Dilantin) experiences an intravenous extravasation. The emergency nurse should in itiate which of the fo llowing interventions after discontinuing the infusion? a) b) c) d) Apply dry heat to the area around the extravasation Manually massage the area around the extravasation Inject calciu m ch loride into the area around the extravasation Encourage patient movement of the area around the extravasation A patient presents to the ED with co mp laints of weakness to bilateral lo wer legs. Assessment reveals the upper arm reflexes are dimin ished. A brief h istory indicates the patient suffered a viral illness approximat ely three weeks ago. The patient is diagnosed with Gu illain-Barre syndrome. Which of the fo llo wing statements , made by the patient, indicates an understanding of teaching given to this patient? a. b. c. d. “I understand that my condition is palliative” “I know that my condition will not affect my cognitive function.” “I can expect to be on antiviral medicat ion for at least four weeks”. “I will return to the hospital or follo w up with my physician if the weakness affects my hands.” Answers: B, A, A, B 10 | P a g e Certified Emergency Nurse (CEN) Exam Review Jeff Solheim ENDOCRINE/ METAB OLIC EMERGENCIES Thyroid Emergencies Mechanism Clin ical Manifestati ons Treat ment _________________________ Elevated thyroid levels _________________________ Decreased thyroid levels • • • • • • • • • Flushing, diaphoresis, hyperthermia Anxiety, tremors, agitation, psychosis Tachydysrhythmias, card iac failu re Tachypnea, pulmonary edema Hypertension Hyperglycemia Abdominal pain Hypercalcemia Metabolic acidosis • • Treat precip itating cause Reverse hyperthermia (acetaminophen, not ASA) fluid and calories Inhibit thyroid hormone synthesis (oral or gastric tube) • Propylthiouracil (PTU) • Methimazole (Tapazole) Slow thyroid hormone release (oral or slow IV) • Iodine (Lugol’s solution) one hour later Beta-blocker to decrease heart rate Digo xin for heart failure • • • • • • • • • • • • • • • • • • • • Hypothermia without shivering Fatigue, lethargy, impaired mentation, seizures, coma Bradycardia Hypoventilation Hypotension Hypoglycemia Flu id retention Dry skin Respiratory or metabolic acidosis Hyponatremia Treat underlying causes (hypothermia, infections, drug overdose) Passive warming Rehydration/sodium replacement Intubation and mechanical ventilat ion for severe hypoventilation. Initiate IV thyroid hormone replacement • Levothyroxine • Thyroxine Hypoglycemia (blood sugar less than 50 mg/dL in adults and 40 mg/dL in infants - note that symptoms may appear in patients with normally high blood sugars which have dropped precipitously at higher serum levels) Clin ical Manifestations Mild hypoglycemia Marked by: Ep inephrine release Clin ical man ifestations Cool, diaphoretic skin Tachycardia Palpitations Shallo w respirations at a normal rate Dilated pupils Moderate hypoglycemia Neuroglycemic symptoms Altered LOC Slurred speech Headache Decreased reaction times Profound hypoglycemia Inability of brain to extract o xygen Disorientation Seizures Co ma Permanent brain damage Treat ment Conscious patient with gag reflex Admin ister 15 g of rapid-act ing carbohydrate and repeat if the patient does not improve within ten minutes Unconscious patient IV dext rose 25 – 50 mL 50% of adults 25% for children 10 – 12.5% for neonates IV o f D5 W Patient with IV Glucagon 1 mg IM (0.5 mg fo r children ages 3 – 5 and 0.25 mg for children < 3 years) May not work for alcohol-induced hypoglycemia 11 | P a g e Certified Emergency Nurse (CEN) Exam Review Jeff Solheim Diabetic Ketoacidosis (DKA ) and Hyperosmolar Nonketotic Syndro me (HNS) HNS DKA Dehydration Profound Less Profound Acidosis None Co mmon Diabetes Type II Type I Blood Sugar > 800 mg/d L < 800 mg/d L Ketones Onset BUN Minimal Days – weeks Extremely elevated Positive Hours – days Mild ly elevated Clin ical manifestations and treatment Effect Clin ical manifestations Treat ment considerations Hyperglycemia Metabolic acidosis Diuresis causing dehydration Electrolyte imbalances Acetone odor to breath Seru m g lucose greater 250 mg/d L Polyphagia Lethargy, weakness and fatigue Weight loss Kussmaul’s respirations Seru m pH less than7.30 Fever Polyuria and polydipsia Tachycardia Hypotension Dry, hyperthermic, flushed skin Dry mucus membranes Poor skin turgor sodium chloride bicarbonate potassium IV insulin (subcutaneous and intramuscular insulin is not utilized because of erratic absorption in the face of hypovolemia) Regular insulin (0.1 unit of regular insulin/kg of body weight followed by 0.1 unit of regular insulin/kg/hour.) Maintain serum d rops at no more than 65 – 125 mg/d L/hour. When serum glucose drops below 250 mg/dL, switch to a dextrose containing solution. Acidosis generally corrects itself as blood sugars are corrected. Normal saline boluses at one liter per hour for 1 – 2 hours followed by 200 - 1000 mL/hour of 0.45% sodium ch loride. (Ch ild ren should receive a bolus of 20 mL/ kg/hour for the first 1 -2 hours) • • • Measure electrolytes at the time of patient arrival and every 2 – 4 hours thereafter. Seru m potassium will usually be elevated and will drop as flu id resuscitation, insulin therapy, and acidosis correction occur. Once serum potassium is < 5 mEq/ L, begin IV potassium replacement to keep levels between 4 and 5 mEq/ L. (insulin therapy may need to be delayed if potassium d rops below 3.3 mEq/L) Replace phosphate and sodium as required. 12 | P a g e Certified Emergency Nurse (CEN) Exam Review Jeff Solheim Adrenal Emergencies Insufficient adrenal hormones is called Addison’s disease. Severe adrenal insufficiency is called Addison’s crisis or adrenal crisis. Factors which can trigger an adrenal crisis Infections Hemorrhage Trau ma Surgery Burns Pregnancy Purpose Adrenal insufficiency Al dosterone (mineralcorticoi d) Reabsorbs water/sodium in the kidneys • Increased urine and sodium loss • Reflex sparing of potassium hyperkalemia and dysrhythmias Cortisol (glucocorticoi d) Increases serum glucose levels • Inhibition of glucogenesis hypoglycemia Hydrocortisone (Solu-Cortef) Dexamethasone (Decadron) Primary treatment • Other treat ment Card iac monitor, IV insulin/dext rose or kayexalate for hyperkalemia • Oxygen, vasopressors and fluids (for dehydration/hypovolemia) Dextrose 50% Cushing’s syndrome (elevated adrenal hormones secondary to prolonged exposure to elevated levels of endogenous or exogenous glucocorticoids). o Sympto ms: Cushingoid appearance Moon facies Buffalo hu mp back Fat above the clavicles Increased risk of: Hypertension Obesity Glucose intolerance Osteoporosis and fractures Impaired immune function Impaired wound healing Patients with Cushing’s syndrome are at risk of developing adrenal crisis if they stop exogenous steroids abruptly. PRACTICE QUES TION Which of the follo wing symptoms of hypoglycemia is considered an “early” man ifestat ion? a) b) c) d) Headache Tachycardia Slurred speech Slowed reaction time Correct Answer: B 13 | P a g e Certified Emergency Nurse (CEN) Exam Review Jeff Solheim REFERENCES American Heart Association. (2010, November). Adult Advanced Cardiovascular Life Support: 2010 A merican Heart Association Gu idelines for Card iopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation , pp. S729 - S767. Baird, M . S., Hicks-Keen, J., & Swearingen, P. L. (2005). Manual to critial care nursing: Nursing interventions and collaborative management. St. Louis MO: Mosby. Beall, B. D. (2005). Salicylate overdose. In E. L. Mitchell, & R. Medzon (Eds.), Introduction to Emergency Medicine (pp. 469 - 473). Philadelphia, Pennsylvania: Lippincott, Williams and Wilkins. Carter, J. S. (2004, November 2). Atoms, molecules, water and pH. 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