Neurology: Knowledge of glasgow coma scale, significance, Neuro assessment including cranial nerves Knowledge and testing of the 12 cranial nerves 1 – Olfactory – sense of smell 2 – Optic – check visual acuity via Snellen Chart 3,4,6 – Oculomotor, Trochlear, Abducens – extraocular movement (H or Pinwheel) 5 – Trigeminal – light touch sensation 7 – Facial – raise eyebrows, clench face, smile, frown 8 – Acoustic – Weber and Rinne Test 9&10 – Glossopharyngeal and Vagus – Gag reflex 11 – Accessory – shrug shoulders against resistance 12- Hypoglossal – stick tongue out Glasgow Coma Scale Rating Significance Increased ICP sign and symptom, treatment choices, meds, and monitoring devices The contents of the skull: Brain tissue—80% Blood----10% CSF----10% This is all the brain can hold Skull bones are fixed, they cant expand. Anytime there’s damage like a tumor that’s growing or if you have injury or tissue swells, so there’s no room to expand so the tissue can die bc it wont get oxygenated. The brain connects to the spinal cord so if the pressure gets to high the brain tissue will go down the spinal cord. This affects breathing. Once brain tissue enters the spinal cord you are basically DEAD. It’s called a brain herniation and compromises all functions of the body. So, we always want to decrease pressure in the brain and prevent it from happening. Monroe-Kellie Hypothesis states that a change in volume of any one component must be accompanied by a reciprocal change in one or both of the other components. If this reciprocal change is not accomplished, the result is an increase in Intra-cranial Pressure (ICP). if there is an increase in any of these 3 there has to be a decrease in a reciprocal of the other two elements within the skull There always has to be a balance If there’s increased blood flow in the brain tissue the CSF amount would have to decrease, and if it doesn’t we would end up with an increased ICP, which can lead to brain herniation. Intracranial Pressure - Intracranial pressure is the hydrostatic force measured in the brain CSF compartment. Acute intracranial problems include disease and disorders that can increase intracranial pressure (ICP) Factors that influence ICP changes are: Arterial & venous pressure Intra-abdominal and intra-thoracic pressure Posture Temperature Blood gases, particularly CO2 levels – how do you think the brain detects blood gases? Baroreceptors (BP) and chemoreceptors (are your oxygen and CO2). If your body detects a low amount of either its going to stimulate the brain to do certain things. CO2 is a major role player for ICP – a normal level is 35-45 and we want to keep it on the lower end of 35-40 Assessment o Changes in LOC o Changes in Vital Signs Cushing’s Triad HTN –SBP, widened pulse pressure (170/50, 180/40, 200/20) and bradycardia (low heart rate) and some books will say a low RR as well, and an increase in systolic pressure. Remember the pulse pressure is the difference btw the systolic and diastolic pressure so if you have an increase in systolic pressure then there is going to be a big difference btw the systolic and diastolic pressure. Tells you that there is a problem in the brain. o Motor changes – contralateral o Pupillary changes/ocular signs – ipsilateral – dilated pupils o Headache/vomiting Respiratory pattern if theres pressure in the brain it compresses the medulla that controls respiratory so you will see changes Remember for Cardiac tamponade Becks Triad: JVD, muffled heart sounds, Low BP Intracranial Pressure Monitoring Normal ICP: 0-15 mm Hg if it gets higher than 15 monitor very closely to see what we have to do to keep it within normal rage Sustained pressure >15 = abnormal ICP HTN > 20 mmHg Associated with increased risk of secondary brain damage Locations for monitoring / measuring ICP: Subarachnoid Space - waveform is dampened due to the bone and tissue- no CSF drainage Intraparenchyma l- in the brain tissue, OK waveform but no CSF drainage Intraventricular - gold standard. Excellent waveform and CSF drainage possible. High risk for infection. Epidural space – Good waveform and CSF drainage is possible. Managing increased ICP Mechanical ventilation: A/C mode is the bed Keep PaCO2 within normal range but the lower end of normal (35-40) Hypocapnia results in cerebral vasoconstriction, while hypercapnia increases cerebral blood flow and therefore the volume of blood within the skull Mechanical ventilation allows us to adjust the settings to achieve normal range. Minimize suctioning/coughing/Valsalva-will raise ICP hence need for sedation and/or NMB o When you cough it increases ICP so you want to suction the pt as needed – you will see the drainage in the tube so make sure to go in and clear the airway – don’t’ do it routinely q2h only when needed A good mode for those pt to be on is an assist control mode so they we can correct the CO2 level When we have a pt with ICP and is intubated we can use the RR to try and keep the CO2 level between 35-45. We will do an ABG to correct the RR on the ventilator When do you get respiratory acidosis? CO2 is accumulating - is a condition that occurs when the lungs can't remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. When do you get respiratory alkalosis? You are in panic mode and hyperventilating - is a disturbance in acid and base balance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide “breathing too fast” If you have a pt on a vent w/ increased ICP our goal is to maintain the CO2 between 35-40 on the low acid side You don’t want the CO2 to become hypercapnic(vasodilation) or hypocapnia(vascoconstriction) If I’m accumulating CO2, what would you do to the RR? Increase the RR to blow off the excess If CO2 is lower than 35, its going to vasoconstrict and further constrict the ability to perfuse the brain. What should you do then? Lower the RR If the person is in an acidotic state their not breathing, so if they were 10 RR on vent go up to 20 and If it alkalotic you drop the RR Look at the Abg and focus on the respiratory rate So if the abg came back and the CO2 is 20 and the respiratory rate on the ventilator is 16, what would you do? Decrease the rate for respiratory alkalosis to decrease how fast they are breathing Suction Prn ICP Monitoring check the drainage for color, it should be clear for CSF, if its not clear then we have a problem. - Nursing care ICP o Rehydrate – I’s and O’s o Decrease stimuli – space out activities o Nutrition, control temperature o Ineffective airway clearance o Ineffective breathing pattern o Ineffective cerebral perfusion o Deficient fluid volume related to fluid restriction o Risk for infection related to ICP monitoring o MAP = SBP +2(DBP) 3 Once you calculate your MAP, I will tell you that the ICP is 15,20,25. Whatever the ICP is you’re going to take the MAP subtract it from the ICP o CPP=MAP-ICP this tells us how well the brain is being perfused CPP normal 70-80 CPP 60-70 monitor closely CPP < 60 will not provide adequate cerebral perfusion and oxygenation. Goal of therapy is to reduce ICP What can you do to make sure ICP isn’t going to increase and the pt won’t further deteriorate? If they have an intracranial drain we don’t want to drain too much at a time. When a doc gives you an order they will say no more than 30cc / hour. Mannitol is the diuretic that we want to use. Bed should be elevated @ least 30 degrees to facilitate drainage. How do we identify early signs of neuro changes? Altered mental status CSF drainage no more than 30cc at a time Decrease edema with osmotic diuretics – Mannitol – it creates a gentle pull of the fluids, so it doesn’t decrease edema rapidly and all of a sudden - Proper positioning to optimize venous drainage keep head and neck aligned, HOB 30 degrees Preservation of cerebral oxygenation and perfusion pay attention to O2 & CO2 level – normal is 35 to 45. If a pt has increased ICP and not breathing well what do you think we put them on? A ventilator bc we can manipulate the respiratory system. The things that we focus on a vent are the type of volume, respiratory rate & oxygen. Tidal volume is the maximum amount of air that a person can take in one breath. Tidal volumes are kept on the lower side 500-750. A normal RR 12-20. Oxygen we can set it up to 100% on a ventilator but they can go higher all depends on the persons condition. The doctor base the setting on what the ABG looks like. Early identification of neuro changes Prevention of complications Surgical interventions Partial lobectomy to remove damaged tissue Hemicraniectomy – bone removed until edema resolved remove the skull and allow the swelling in the brain to go down, and then reattach it later – this is to prevent the herniation. This is the last resort. We paralyze them while on a vent to not have them do anything and correct the CO2 levels Complications of ICP Tissue ischemia Tissue compression (herniation) Diabetes Insipidus vs. SIADH o - - - SIADH water retention give diuretics & labs diluted Results when high ADH production occurs resulting in excessive water retention Results when high ADH production occurs resulting in excessive water retention o Lead to cellular & cerebral edema, dilutional hyponatremia o Pt has fluid retention - increased weight but no edema, low serum osmolality concentrated urine, dilutional hyponatremia - ‘holding on’ to fluid (Hemodilution) Diag: Low serum osmo, high urine osmo, Low NA, Low Hct RX: Restrict fluis, Hypertonic saline IV, Monitor & correct Na & treat underlying cause Pressure in the brain is going to impact all the tissue and especially the endocrine system (pituitary gland, which secretes anti-diuretic hormone – posterior part) ADH regulates water, if you have too much you retain a lot, getting edematous, labs become diluted, low sodium, concentrated urine and serum results, fluid overload, hyponatremia, which will lead to issues in the brain such as seizures, irritability. If they have low sodium give them (couldn’t make out the name of the drug) give it with a lot of caution. Hypertonic solution IV gradually. 3 % saline. We want to stabilize Na levels and restrict fluids, may use diuretics w. caution bc electrolytes are already imbalanced. o DI losing fluid & dehydrated - - - Results when there is insufficient ADH produced, resulting in increased loss of free water, dehydration, thirst. Make sure to correct sodium and give them fluids bc they are severely dehydrated. S&S Fluid and electrolyte imbalances occur: caused by increased dilute urinary output (low urine specific gravity & osmolality (5-24 L/day) Plasma osmolality is INCREASED due to hypernatremia and dehydration. Concentrated labs S&S of shock/dehydration Diagnosis o High serum osmo & low urine osmo o ADH levels o H&H, Na, BUN RX: o Rehydrate, I&O o Replace ADH Sometimes pts will have projectile vomiting Cushing triad, Battle sign, de-cerebrate vs. decorticate posturing Battle’s Sign Bruising on the mastoid process indicating a skull fracture something that you’re going to see on the mastoid a bluish discoloration – some bleeding in the ear, bruise or echimosis behind the ear Cushing Triad Hypertension, widended pulse pressure, bradycardia Cushing’s triad: HTN –SBP, widened pulse pressure (170/50, 180/40, 200/20) and bradycardia (low heart rate) and some books will say a low RR as well, and an increase in systolic pressure. Remember the pulse pressure is the difference btw the systolic and diastolic pressure so if you have an increase in systolic pressure then there is going to be a big difference btw the systolic and diastolic pressure. Tells you that there is a problem in the brain. Significance of patient posturing Decorticate goes to the core and Decerebrate goes away from the core. Decorticate is when a pt is having increased ICP, and there is still a chance to save them. Once you see Decerebrate the level of damage is too much in the brain. Responding to pain you can say its either localized when you pinch them. A pt that’s comoatose or flaccid will have no response to that. - Decerebrate away from the core – damage to bad in the brain o One or both arms stiffly extended o Possible extension of the legs - Decorticate towards the core- can still save o One or both arms in full flexion on the chest o Legs may be stiffly extended Spinal cord injury, complications and nursing considerations. Incomplete - Retention of all or some or some of the motor or sensory function below the level of injury Complete - Total loss of voluntary muscle control and sensation below the level of injury suggests that the lesion is complete o C1 to T1 quadraplegia o T2 – L1 parapplegia Central Cord Syndrome - Centrally located damage - Hyperextension of the cervical spine often is the mechanism of injury - Damage greatest to the cervical tracts supplying the arms - Clinically, the patient may present with paralyzed arms but no deficit in legs or bladder Brown-Sequard Syndrome - The damage in this syndrome is located on one side of the spinal cord Loss of motor function, position, vibratory sense, and vasomotor control on the SAME side of the injury –ipsilateral - Loss of pain and temperature sensation below the level of the lesion on the OPPOSITE side – contralateral Anterior Cord Syndrome - The anterior aspect of the spinal cord is damaged Patient usually has a complete motor paralysis below the level of injury and loss of pain, temperature, and touch sensation Posterior Cord Syndrome - Result of a hyperextension injury at the cervical level – rare Position sense, light touch, and vibratory sense are lost below the level of the injury o o o o Central cord syndrome- arm paralysis Anterior cord syndrome -motor paralysis Posterior cord syndrome- sensory paralysis Brown-sequard syndrome- loss of motor on the same side of injury and loss of sensation on the opposite side C-Spine Injuries - C2-c3 usually fatal C4 is major innervations to diaphragm - C4 = paralysis of 4 extremities - C5 may have movement of shoulders - C3-c5 is greatest risk for impaired spontaneous ventilation – phrenic nerve - Tetraplegia = quadriplegia Thoracic Injuries - Loss of chest, trunk, bowel, bladder, and legs may occur - Lesions/injuries above T6 associated with autonomic dysreflexia Complications - Spinal shock o Loss of motor, sensory, reflexes and autonomic activity below the level of injury caused by the sudden cessation of impulses from the higher centers o Can last days, weeks, or month o Cord shuts down as the body’s response to assess damage o Impossible to assess full damage until deep tendon reflexes return - Neurogenic shock o Loss of vasomotor tone due to injury and loss of sympathetic innervation and results in hypotension, bradycardia, and warm dry extremities o Associated with high thoracic injuries o Causes cellular ischemia Treat with vasoconstrictor since patient is hypotensive – want to force blood out - Autonomic dysreflexia o Syndrome that affects T6 and above o Provoked by negative stimulus – full bladder or bowel, heat/cold o Characteristics include severe hypertension, and bradycardia with flushed upper body and pale lower body o Danger of seizure or stroke o Hypertension – SBP may get to 300 o Bradycardia – 30 to 40 BPM o Flushed face and neck, sweating (pilomotor reflex) – only above the level of the spinal injury; below will be cool and dry o Severe pounding headache, nasal stuffiness, dilated pupils, blurred vision, nausea and restlessness Nursing care - - Do not move them if you don’t know if they have a spinal cord injury or not!!! Prevent further damage, immobilize and stabilize Prevent ischemia – treat shock, hypoxia, swelling High dose of methylprednisolone initially and during early hourse Prevent or treat complications o Chronic disability, spasticity, DVT, Decubitus ulcer, Curling’s Ulcer, Aspiration, pneumonia ABCD o Airway with C-spine collar o Breathing, pay attention to cervical area and intercostal muscles o Circulation, including checking pulses, stop external bleeds, IV access o Disability, neuro exam for responsiveness, pupil checks, motor/sensory deficits Bowel and bladder help Psychosocial promotion Safety from falls - Skin/ulcer prevention Temperature regulations – have decreased ability to sweat and shiver Spinal shock vs. neurogenic shock vs Autonomic Dysreflexia. – listed under spinal injury complications Basilar Skull Fx sign and symptom and tx options and nursing considerations. - Check for Battle’s Sign Check for rhinorrhea or otorrhea Check for glucose from nasal/ear drainage High risk for carotid rupture EVER place a nasogastric tube in a patient with a basilar skull fracture!! Bc the tube can end up in the brain-pt can die Strokes and TIAs Ischemic - - - a clot that stops blood supply to an area of the brain Treatment o Thrombolytic therapy within 3 hours of symptom onset o Anticoagulant/antiplatelet therapy o Management of increased ICP and cerebral edema o BP management o Strict glycemic control – hyperglycemia can increase cerebral edema o Fever control/induced hypothermia o A pt that has a stroke you always want to ask them: smile for me, hold your hands out, look at the face, see how they respond, and ask when the symptoms started. o If she went to bed and her husband says she was fine when she went to bed, and when she woke ups he was talking crazy – do you know exactly when that stroke happened? No, so don’t give TPA bc we don’t have a time frame – the longer you wait to use it the higher the risk of bleeding o If you suspect a stroke the first thing you do is a CT to see what kind of stroke it is You find out that it is an embolic stroke after the CT scan – what do you do? Give TPA, and before you give it you want to check your absolute & relative contraindications. The moment the pt tells you I’ve had a brain tumor in the past or any kind of head trauma or severe facial trauma, major sx within the last 3 months – are all contraindications to giving TPA. They will bleed. DON’T GIVE TPA if they have any of those contraindications. As soon as the person has chest pain and you think that they have an MI the first thing you are going to do is give them aspirin & hook them up to an EKG and troponins TPA calculation You have a pt that is going to get activase (tpa). Tpa is usually given over 60 minute, that is standard protocal o o o The total dose to be infuse over 60 minute is 58.5mg Bolus: 5.85 or 6ml given over 1 minute Remaining Infusion: 52.5 ml/hr be to infusion in 59 minutes MERCI - Nursing Care Hemorrhagic can lead to increased ICP – life threatening, pts can die from it and can happen due to congenital deformities When blood leaks into the brain tissue Treatment o BP control – not too high/low o Aneurysm precautions Quiet environment, stool softeners to prevent straining, limit visitors o Elevate HOB 30 degrees o Pain control for headache o Surgical repair if possible o Prevention of vasospasm More dangerous bc its more lethal Embolic stroke has a better prognosis where as a hemorrhagic stroke we might not save this pt. A hemorrhagic stroke can happen due to a high BP or an arterial venous malformation or an aneurysm (a bulging in the arteries and can burst- as long as its small and the bp is controlled we’re ok but if the size starts to increase we’re in trouble) Stroke means and area of the brain is getting blood, so no oxygen, so it can die When it is going to die the whole brain doesn’t just shut off – you have layers and some of the tissue will start to die and other areas will be almost going to die. The areas that are almost going to die you do a CT and giving TPA this is the area you are saving – the medical term is “conomra” How is a stroke different from a TIA? It’s very short lived < 24 hrs – A transichemic attack. They don’t find a thrombus or emboli on the CT scan but pt can present with weakness so the pt will just be monitored for the next 24 hours. And the next day you’re ok with no weakness. This is a warning sign that if the pt doesn’t modify the modifiable factors they are at risk for a real stroke. So, the pts that we want to salvage the conomra we want to give thrombolytics within first 3 hours, anticoagulants to prevent clots, prevent s/s of increased ICP so asses for altered LOC w/ glasgowcoma scale, HTN verly closely monitored o this is the first initial complaint and can kill you in a matter of minutes ACT QUICKLY. Once it ruptures it can destroy the BBB which protects unwanted things from entering the brain, and then anything can come and alter the equilibrium in the brain and lead to increased ICP. If it’s a small bleed we can save you if it’s a massive bleed odds are that you are going to die. If it’s a small bleed and BP is the biggest issue we lower the BP with nitroproside(don’t use it so much bc it has a complication for syianide toxicity) /cardine for the neuro to prevent the spasms. Tumors, subdural hematoma, epidural hematoma (S & S and Treatment choices) Subdural hematoma - occurs from bleeding between the Dura matter & Arachnoid layer of the meninges results from injury to the brain substance and its parenchymal vessels venous in origin – hematoma develops slowly LOC, ipsilateral pupil dilation, contralateral weakness, personality changes acute o manifests signs within 48 hours of injury o treatment: crainiotomy, evacuation, decompression subacute o manifests 2 to 24 days of the injury o treatment: evacuation and decompression chronic o develops over weeks to months o peak incidence is around age 50-60 due to brain atrophy o treatment: evacuation and decompression Venous system is a slow pressure, this is all your A. fib pt or anybody that has a bad bump to the head and they look fine and feel fine and they didn’t do a CT scan bc they thought everything was ok but if there is a venous bleed, blood is going to increases and put them in a coma if its not picked up. Subdural hematoma is a slow bleed, but it can be deadly if it’s not detected. Bc anytime you increase the volume in the brain it going to cause increase ICP and herniation. These pt may have LOC impair, muscle weakness, sensory weakness, difference in the pupil reaction. Bc it a slow bleed we can watch and wait, they call it watchful waiting. We are looking to see if it will be reabsorb, or is it small enough to manage medically or do we have to go in and do the surgery to remove the bleed. So the first thing we do is watchfull waiting but if they are showing S/S tx w/evacuation An older pt that has A.fib and is on a blood thinner, and also lives alone comes in after a head injury that happen a couple of day. They present with slur speak and LOC its usually do to subdural hematoma Epidural hematoma - results from bleeding between the Dura and the inner surface of the skull requires immediate surgical intervention! Associated with a linear fracture crossing a major artery in the dura, causing a tear Unconsciousness with brief lucid intervals, followed by decreased LOC Other manifestations include headache, nausea and vomiting Treatment o Rapid surgical intervention SAH and other strokes, diagnostics, treatment modalities, nursing assessments, and types of aphasias. Diagnostic Tests - CT o o - - - Done first when suspected stroke to figure out type Instruct the patient to lie flat on a table with the machine surrounding, but not touching the area to be scanned o Patient must remain as immobile as possible – sedation may be required o The scan may not be of the best quality if the patient moves during the test of if the X-ray beams were deflected by any metal object Lumbar Puncture o Cerebrospinal fluid analysis o Inserted between 3rd and 4th Lumbar Vertebrae o Position on side with knees and head flexed, some pressure may be felt – tell them to not cough or move o Keep patient flat for 8 to 10 hours to prevent headache and encourage fluid intake o Never ever perform a lumbar puncture on a patient with elevated Intracranial Pressure or a patient who is coagulopathic Cerebral Angiogram o Illuminated the structure of the cerebral circulation o Pathways are examined for patency, narrowing, and occlusion as well as any structural abnormalities such as aneurysms, vessel displacement caused by tumors or edema, and alterations in blood flow from tumors or arteriovenous malformations o A local anesthetic will be used for insertion site of the catheter – usually femoral artery o A flushed feeling will occur when the medium is injected o After assess site for swelling, redness and bleeding o Check the skin color, temperature and peripheral pulses of distal extremities o A large amount of contrast may be needed during the test with can result in increased osmotic diuresis and risk for dehydration and renal tubular occlusion o Temporary or permanent neurologic deficit anaphylaxis, bleeding, hematoma, and impaired circulation to extremity may occur Blood and Urine test Gastrointestinal/Liver disease/Pancreatitis: GI trauma/bleeds (treatment options, Cullen’s sign, Grey Turner sign, and nursing care). If the pancreas rupture into the peritoneal cavity and there’s bleeding these are the two signs well see first: Grey-Turner’s and Cullen’s signs signal hemorrhagic pancreatitis. o Cullen’s signs- circular bruising around umbilicus o Grey-Turner’s- bruising on flank sign of patient body. Need to turn patient to look for this Clinical Manifestations Severe, unrelenting left upper quadrant (LUQ) pain (epigastric) that radiates through the back (sudden, severe, deep, piercing and steady (aggravated by fatty meals, alcohol or lying flat) o The moment you put something on your tongue your salivary gland act and send an impulse to the brain to tell the pancreas to secret enzyme- NPO to prevent the enzymes from releasing Abdominal tenderness and guarding N&V and weight loss Absent or decreased bowel sounds UPPER GI BLEEDING- Sources: esophagus, stomach, duodenum Assessment of UGI Bleeds History o Previous bleeds, epigastric pain, ETOH, vomiting, retching, coughing Physical Exam o Change in CV status Signs/symptoms of shock or hypovolemia o Mental status changes o Board-like rigid abdomen – peritonitis Laboratory/Diagnostic studies o CBC, electrolytes, BUN, PT, liver enzymes, ABG, T&C, stool & vomitus for gross and OB, U/A (SG) o Endoscopy; Mesenteric angiogram Management of UGI Bleeds Two large-bore IVs o Fluids- isotonic o Blood products (TCM for 4 units of PRBC) Monitoring * Tissue perfusion- CVL, PA cath * Labs o UOP NPO Activity as tolerated Classic Symptoms Hematemesis-vomiting o Indicates bleeding above the ligament of Trietz o Bright red indicates active, profuse bleeding- this could indicate a varices has ruptureupper GI o “Coffee-ground” emesis is RBCs broken down with HCL acid, causing it to turn brownduodenal area Hematochezia-stool o Usually indicates lower GI bleeding o Blood is a cathartic and moves rapidly through the system o Can indicate upper GI bleeding if bleeding is massive Melena o Blood in the stools that turns them black (tarry) and foul smelling o Indicates upper GI bleeding in 90% of cases o May take several days to clear stools o Stools will remain positive for occult blood for 1 to 2 weeks (detected by positive guaiac test) Lower GI Tract Bleeding Small intestines, colon, anus Board-like rigid abdomen – peritonitis, bowel sounds not present Ranges from microscopic to massive hematochezia Large volume hematochezia (passage of maroon-colored stool). requires hospitalization Surgery may be required o Most common causes infectious colitis, anorectal disease, IBD, diverticulosis, neoplasms, rectal ulcers, NSAID use, colonic varices Symptoms- constipation, cramping, pain, rectal bleeding-bright red blood if new and black (melena) if old. Lower GI Bleed Diagnostics and Treatment Colonoscopy Sigmoidoscopy KUB CBC Biopsy if indicated Transfusion IV fluids Surgical intervention (bowel resection, hemorrhoidectomy etc) Nursing concerns about cirrhosis and its complications of esophageal varices, hemorrhage, portal HTN, ascites, and encephalopathy). Lab data, medications, and tx considerations Diagnostic procedures (prep and post care and nursing considerations) HEPATIC CIRRHOSIS- NEED TO KNOW There injury to the liver. Kupffer cells are damage and it could lead to scarring Four causes of cirrhosis: 1. Alcoholic or Laennec’s cirrhosis- biggest cause- Fatty deposits are laid down in the liver. Widespread scar formation results. This is reversible if the individual stops drinking alcohol before cirrhosis occurs. 2. Post-necrotic cirrhosis-complication of viral, toxic, or hepatitis that wasn’t manage well. Broad bands of scar tissue form within the liver. 3. Biliary Cirrhosis- gallbladder blocked up and wasn’t draining well and backed up into the liver causing fibrosis. associated with chronic biliary obstruction and infection. Diffuse fibrosis of the liver. 4. Cardiac Cirrhosis-results from long-standing severe right heart failure in patients with cor pulmonale, constrictive pericarditis, and tricuspid insufficiency. Symptoms Weight loss, fatigue Bruising, bleeding Petechiae (Spider angiomas or spider nevi) • Spider nevi • Hormonal changes Palmar erythema (red area that blanches on palms)-due to increase in circulating estrogen and the liver is unable to metabolize steroid hormones Elevated liver enzymes-SGOT, SGPT, ALKP, bilirubin, PT Anemia, thrombocytopenia Leukopenia Decreased albumin levels Increased ammonia levels (confusion, coma) Peripheral neuropathy (asterixis-also known as “liver flap” due to elevated ammonia levels) Jaundice-results from the inability to conjugate and excrete bilirubin Esophageal Varices: NEED TO KNOW Usually form as a result of liver cirrhosis. Complex of tortuous veins at the lower end of the esophagus. Swollen and engorged due to portal hypertension. Varices contain little elastic tissue and are quite fragile. May rupture as a result of coughing, sneezing, vomiting etc. A big deal because you can’t reach it to stop it o Patient comes to the ER vomiting blood the biggest priority is airway! If they need help breathing then Incubate first then address the source of the bleed Treatment 1. Esophageal tube (EGD) with camera to look at the area and catharize(stop bleeding) it 2. Inject medication (Vasopressin, epinephrine, octreotide) – NEED TO KNOW Powerful vasoconstrictor- when we eject vasopressin into a bleed it constricts and stop the bleeding Ask pt about pass medical history bc If a patient has angina don’t give them vasopressin. 3. Sengstaken-Blakemore Tube (3 ports) Interventions: Gastric lavage Instilling large volumes of water or normal saline into stomach via a large bore tube Fluid removed after instilled either by gravity or suction Purpose is to localize site of upper GI bleeding, evaluate bleeding, cleanse stomach, prevent aspiration, prepare for endoscopy Endoscopic Therapy EGD. May perform scleral endoscopic therapy-injection of sclerosing agent directly into vessel or use of heat. Epinephrine commonly used— causes vasoconstriction and stops bleeding. Goal: coagulate or thrombose the bleeding vessel o Thermocoagulation o or laser o Epinephrine o EVL- Endoscopic Variceal Ligation Blakemore Tube Sengstaken-Blakemore Tubeo A SPECIAL TYPE OF NG Tube Tube is inserted by the doctor. This is one tube the NURSE does not manipulate The purpose of this is to create pressure at the junction of esophagus. Majority of the esophageal varices occur there o It has two balloons, Gastric and esophageal balloon o Gastric balloon= anchor in the stomach so it doesn’t move up. Inflate balloon to keep it o Esophageal = tamponade. When inflate it compress on either side of the varices to prevent it from bleeding o Kept in for 2-3 days and no longer because it can cause necrosis of the area because it won’t perfuse properly o If gastric balloon ruptures, esophageal balloon can migrate upwards and occlude airway- If gastric balloon lose air or is not anchor properly it can migrate up. Can block the airway. If it gets out of place call the doctor o Can also cause ischemia o Elevate HOB o Keep Scissors and syringe at bedside- if patient is choking because the balloon is blocking traches you can cut tube and it deflate instantly Care Mouth care Suction at bedside Prevent dislodgement Maintain balloon pressures Assess for esophageal rupture Sedation, emotional support ENCEPHALOPATHY-NEED TO KNOW Neurological changes caused by hepatic failure- related to increased levels of ammonia BUN/protein not metabolized by liver = increased ammonia level -> changes in LOC. Patient will quickly progress to coma and death if ammonia level is not lowered. Treatment • Diet* - Consume protein in low amounts. You don’t want to eliminate protein bc you still need protein in your protein. Educate family that Too much protein makes the confusion worse and can lead to a coma. So your job is to provide the necessary amount of protein without impairing the neuro function. • • Lactulose (causes diarrhea) • Neomycin Normal ammonia level (NH3) 15-45 mcq/dl (Varies by institution) Symptom Monotonous speech Drowsiness Confusion, delirium, coma Fetor hepaticus (“breath of the dead”) Asterixis is a warning sign- tremor of the hand when the wrist is extended, sometimes said to resemble a bird flapping its wings. Cerebral edema will develop in 75-80% of patients with grade IV encephalopathy Hemorrhage in liver failure Due to many significant hematologic changes. Liver not producing coags Splenomegaly results from backup of blood from portal vein leading to thrombocytopenia, leukopenia and anemia. Failing liver is unable to produce prothrombin and other essential clotting factors. Bruising, petechiae, bleeding Note on blood products If the patient is bleeding due to an elevated PT, which blood product must be given? FFP If the patient is bleeding due to thrombocytopenia, which blood product should be transfused? Platelet Low platelet count gives platelets. Treat less than 100,000 Give fresh frozen plasma (FFP) when there’s low clotting factors and when PTT and INR is high Give blood when hemoglobin is low PORTAL HYPERTENSION- NEED TO KNOW Increase in portal venous pressure with vasoconstriction- scaring increases the pressure in portal veins o Blood cannot enter the liver, so it shunts away from down other channels Bleeding of esophageal varices major complication Other noted problems associated with portal hypertension: o -Immunologic alterations (splenomegaly) o -Fluid alterations o -Ascites o -Alterations in hormone and fat metabolism Esophageal Varices Due to portal hypertension Treatment: Avoid irritants, coughing Medications: Vasopressin (Pitressin) Aquamephyton (Vit K), BetaBlockers Endoscopy Tamponade (Blakemore tube) Transjugular Intrahepatic Portosystemic Shunt (TIPS) o Procedure of choice for varices- Controls bleeding by decreasing portal venous pressure & decompression of portal system o Involves placement of a stent between portal and systemic circulation to redirect blood flow. Creates shunt to Bypass the area that’s area that is necrosis so the liver could still get blood. WE NEED TO DIVERT BLOOD FLOW o LOOK AT THE QUESTION. IF IT SAYS: WHAT ARE YOU DOING FOR THE PATIENT INITIALLY? WE FIRST START WITH MED. NEXT SEE IF WE COULD CARTHRIZE. NEXTINJECT MEDCATION. NEXT BLAKEMORE TUBE. WE DO NOT GO TO TIPS RIGHT AWAY!! ITS NOT SOMETHING WE DO FIRST. TIPS is for long term for alcoholic patients who keep having repeated esophageal varices EDEMA/ASCITES Low albumin + high portal vein pressure o Low albumin means most of the fluid is going into third spacing o Replace protein gently, in low amount because we don’t want patient to end up with hepatic encephalopathy Weight- is the best indicator. Before procedure weight patient then after a paracentesis weigh then TreatmentParacentesis Hepato-renal Syndrome If the liver doesn’t filter and detoxify waste products, then the kidney has to work harder. And if liver is not perfusing properly chance are the kidney is not going to get the same amount of blood and oxygen patients require both a liver and kidney transplant Pancreatitis S&S and common concerns and complications ACUTE PANCREATITIS- NEED TO KNOW CAUSES: Gallstones, excessive ETOH (70% to 80%), drugs, ERCP PATHOLOGY: With acute pancreatitis is when the pancreases enzymes open up in the pancreas and digest itAUTODIGESTION OF PANCREASES Premature activation of pancreatic digestive enzymes before release in duodenum. All etiologies, however, show premature activation of digestive enzymes-autodigestion. In essence, the pancreas eats itself. Associated with systemic inflammatory responses Can be life-threatening o If not caught early, it causes develop into PERITONITIS o Travel up to the lungs and development of ARDS and Pleural effusion (chest tube or thoracentesis) A common mnemonic for the causes of pancreatitis spells "I get smashed", an allusion to heavy drinking (one of the many causes) I - idiopathic. G - gallstone. MAJOR CAUSE Gallstones that travel down the common bile duct and which subsequently get stuck in the Ampulla of Vater can cause obstruction in the outflow of pancreatic juices from the pancreas into the duodenum. The backflow of these digestive juices causes lysis (dissolving) of pancreatic cells and subsequent pancreatitis. E - ethanol (alcohol) MAJOR CAUSE T - trauma S - steroids M - mumps (paramyxovirus) and other viruses A - autoimmune disease (Systemic lupus erythematosus) S - scorpion sting (e.g. Tityus trinitatis), also snake bites and brown recluse spider bites H – hyperlipidemia/hypertriglyceridemia and hypothermia, HYPERCALCEMIA o Hypercalcemia- can lead to pancreatis. But when you check the labs it shows hypocalcemia, why? Because once you have the enzyme is being release, they bind to calcium causing hypocalcemia. Danger signs: Chvostek and Trousseau. E - ERCP (Endoscopic Retrograde Cholangio-Pancreatography) D - drugs (SAND - steroids & sulfonamides, azathioprine, NSAIDS, diuretics) LABS & Diagnostics: Elevated pancreatic enzyme levels; elevated glucose & triglycerides; decreased calcium in severe disease; CT Abd LABS: >WBC, >glucose, >bilirubin, >> alkaline phosphatase, >urinary amylase >AMYLASE, >LIPASE (elevated) Presentation: Acute abdominal pain, severe knife-like and steadily increasing, unable to lie flat; nausea and vomiting, abdominal distention; persistent fever, leukocytosis. Signs of hypovolemia from massive fluid shifts (Tachycardia (first sign), Tachypnea, **Pain, Hypotension, Dehydration). If there is bleeding in the pt body and these is no other cause, sinus tachycardia is the first sign If the pancreas rupture into the peritoneal cavity and there’s bleeding these are the two signs well see first: Grey-Turner’s and Cullen’ GI feeds vs TPN Enteral NGT o o o o PEG o Precautious: aspiration Keep HOB up 30 degree Check for diarrhea, that means the patient is not tolerating feeding Check residual q4h- flush tube after Goes through jejunum or lower part of the stomach Parenteral (IV feedings) Not really preferred because they rather someone having enteral so they can use their gut and keep it going Glucose control paramount when utilizing PPN / TPN— may need insulin drip PPN o Large peripheral vein (basilic vein) o Short term for prevention of malnutrition o Peripheral line o Glucose content is lower o Lower osmolality o Monitor for hyperglycemia and infection o Short term for prevention of malnutrition TPN o Central venous access (superior vena cava or internal jugular) o Needs central line Triple lumen catheter: one line is dedicated to TPN only- don’t break it for any medication. Lipid can be piggy back into the line. These are the only two things allowed in the line If all three lines are being use and you need to start a TPN you need to start a separate line or start another line o o o o Liquids food in a bag is the only thing that’s in conjunction with a TPN Glucose content is higher Higher osmolality Monitor for hyperglycemia (blood sugar monitoring) and infection because sugar attracts bacteria (check WBC). Anytime you disconnect or reconnect it increase the chance of infection o Hyperglycemia crisis can occur if TPN is giving to fast, can also cause fluid overload o Longer term & for higher protein & caloric requirements o Long term therapy with TPN can lead to liver failure If patient is at risk for aspiration give them a one-time bolus feed Continuous feed Glucose control paramount when utilizing PPN / TPN—may need insulin drip Tube clogging o Warm water mixes for medications o ALWAYS flush tube well after medication administration. Check with pharmacy for liquid form if possible. o If SBFT gets clogged, can use “clog-zapper” to unblock. Also, Coca-Cola or bicarb. Appropriate GI meds, precautions, etc. Treatment- NEED TO KNOW the mechanism of action, the purpose, and what to look out for PPIs (proton pump inhibitors) o Esomeprazole o Lansoprazole o Omeprazole o Pantoprazole o reduce the production of acid by blocking the enzyme in the wall of the stomach that produces acid o block the hydrogen ion pumps o Suppresses H, K–ATPase enzyme system of gastric acid secretion o These come in capsules tell patients not to open it Antacids o Alka-Seltzer o o o o Milk of Magnesia Pepto-Bismol Tums Mylanta o If Increase pH of gastric contents by deactivating pepsin o If you have too much acid in your stomach (low pH) we can give these to neutralize the pH. o They contain ingredients such as aluminum, calcium, magnesium, or sodium bicarbonate which act as bases (alkalis) to counteract stomach acid and make its pH more neutral. o Aluminum and Calcium look for constipation o Magnesium look for diarrhea Cytoprotective agents o Sucralfate (Carafate) can heal an active ulcer, but it will not prevent future ulcers from occurring. o Misoprostol (Cytotec) Not good for pregnant women o Lining of the stomach by adhering to ulcer sites and protecting them from acids, enzymes, and bile salts. Carafate is used to treat an active duodenal ulcer. H2 Blockers o Nizatidine o Famotidine o Cimetidine o Ranitidine o Short term use o Decreases gastric acid secretions by blocking histamine receptors in parietal cells o Cimetidine is very toxic. When giving it to older people asses their mental status closely because it can make them confuse Antibiotics for H. Pylori o Metronidazole (Flagyl) o Tetracycline o Take 2 weeks to a month Nausea o Ondansetron o Metoclopramide (Reglan) Diarrhea o Imodium (loperamide) o Kapectate (bismuth subsalicylate) o If you take too much you can end up with constipation Vasopressin drip—splanchnic vasoconstriction. o Observe pt for cardiovascular side-effects including chest pain. o Sandostatin (octreotide) drip-decreases splanchnic blood flow and HCL acid production. o Epinephrine Surgical resection may be required (oversew) NGT placed to gravity or very low suction (high suction will further damage mucosa and dislodge clots) Iced water NG lavage still used occasionally—cold water instilled into NG tube causes vasoconstriction.
