Management of Traumatic Brain Injury and Spinal Cord Injury, Exams of Health sciences

Download Management of Traumatic Brain Injury and Spinal Cord Injury and more Exams Health sciences in PDF only on Docsity! Page 1 Critical Care Exam 3 Guide latest Update Download to Pass Neuron Basics · Brain metabolism o Soul source of energy for the brain is glucose. Brain needs glucose to function. Brain cannot store it, but needs a constant supply. If glucose levels start to fall you will some changed. o Cerebral glucose < 70 mg/dL = confusion o Cerebral glucose < 20 mg/dL = damage · Cerebral blood flow · Autoregulation o Changes in pressure o Changes in CO2 ▪ Alters cerebral blood volume with change in blood vessel size o Ability of the blood vessel in the brain to either constrict or dilate in response to pressure or CO2 levels ▪ Hypotension or hypo ventilating causing hypercapnia BV in brain will dilate and vice versa try to send more blood and oxygen to brain. ▪ If hypertension or hypocapnia blood vessels in the brain will constrict. ▪ Systolic less than 50 or greater than 160 BV in brain lose the ability to autoregulate. Neuro Assessment o GCS, LOC, Memory, speech, Reflexes (Babinski with brain injury) which only babies should have if adult has it this is not good, motor response, sensation , look for aphasia, motor strength Page 1 of 53 Page 2 ▪ Concerned with GAS or 8 or lower o Posturing ▪ Decorticate · Extremities go toward the body ▪ Decerebrate · Extremities pull away from the body, more severe, damage to brainstem – this is the worse posturing · Cranial nerves o 1 – Olfactory - Smell o 2 – Optic - vison, pupil response, visual fields – PERRLA - need flashlight or pen light dim the lights in room o 3, 4, 6 - Oculomotor, Trochlear, Abducens - eye movement – 6 fields of gaze “EOM’S” Page 2 of 53 Page 5 · Optimal is 70-100 mmHg · If less than 70 you can develop ischemia to brain tissue. · If under decrease BP or increase ICP ▪ If CPP is inadequate, ischemia or infarction can occur · Increased Intracranial Pressure o Associated with many neurological problems o ICP 20mm Hg or greater for 5 minutes or longer Increased metabolic de- minds, fevers, seizures can also increase in- tracranial pressure. o Results from an increase in any one of the three com- po- nents: ▪ Increased Blood Volume · Loss of Autoregulation · Decreased Oxygenation · Hypercapnia – cause blood vessels in brain to dilate sending more blood to brain which can increase pressure · Obstruction – Ex: Tumor ▪ Increased Brain Volume · Cerebral Edema ▪ Increased Cerebrospinal Fluid · Hydrocephalus o Cardinal (early) sign is changes in LOC Page 5 of 53 Page 6 o Pupil changes, respiratory changes are late sign o Herniation = he dead ▪ Brain usually comes out of foramen magnum ▪ Nurse needs to identify signs early. Prevention es may important. ▪ If ICP > 20 for 5 minutes or more herniation can occur. ▪ We need to know the signs to look for to prevent herniation to occur. ICP Monitoring · Indications o Severe head injury, severe neurologic disorder, GCS < 8, Post brain surgery, tumors, strokes · Purpose Page 6 of 53 Page 7 o Severity of brain impairment, diagnose problems, assess responsiveness to therapy, au- mint our assessment · Placement o Most placed in the ventricle because you can drain CSF also o Mostly placed in OR but can be placed at bedside o Only placed by neuro surgeon. · Transducer System o Fluid Filled o Microchip o Fiberoptic Catheter o Monitors can be placed in different areas of the brain, but most monitors will be places in the ventricles, most of these monitors have the ability to drain CSF as well. · Nursing Management o During Placement ▪ Set up equipment ▪ Maintain asepsis ▪ Dress the site after its been placed ▪ Document o During ICP monitoring ▪ Hourly neuro checks, hourly vitals (MAP, ICP, CPP), maintain sterility, monitor form complications (hemorrhage, infection), biggest complication is infection. Huge risk is also meningitis. · Cerebral Oxygenation Monitoring o Jugular Oxygen Saturation ▪ Monitored via a fiberoptic catheter ▪ Normal value 60%-70% · Does not ensure adequate perfusion Page 7 of 53 Page 10 · Suctioning o Only when necessary because it increases ICP o Preoxygenate beforehand. o Limit suction to 10 seconds. No more then 2 to 3. · Assessment o Neurological exam hourly. o Vital signs Page 10 of 53 Page 11 ▪ Cushing’s triad (bad) – never want to see this. ICP is so high that it is putting pressure on brainstem. · Hypertension, Bradycardia, Abnormal respiratory rate and pattern · Last thing before the patient herniates · If patient has this. Sit the patient up as high as possible (high fowlers). Patient will need surgery there is not much the nurse can do. · Nursing activities o Avoid clustering of activities o Avoid valsalva situations ▪ Pooping, coughing, vomiting. Can give stool softeners for poop. Vomiting can put in NG or give them an antiemetic. o Minimize external stimuli ▪ Noise, light, activities. No more than 2 family members in room. Keep it quiet. ICP Medical Management · Adequate Oxygenation o Goal: PaO2 > 80mm Hg o Maintain O2 and CO2 levels. o Airway vigilance o Mechanical ventilation o Use PEEP with caution – decreases venous returns. If not in heart could be in brain because it’s everywhere. Typically won’t see more than 5 of peep. o Adequate hematocrit · Carbon Dioxide Management o PaCO2 35-45 mm Hg o Avoid hyperventilation unless you see Cushing Triad. · Diuretics Page 11 of 53 Page 12 o Osmotic and Loop diuretics ▪ Reduce brain tissue volume (cerebral edema) · Mannitol – drug of choice, crosses BBB – pulls the sodium and water out of the brain tissue so you can pee it out) · Hypertonic saline (use caution and patient must have a central line) 2nd choice and keep a close eye on sodium level. · Steroids o Dexamethasone – also known as dead-on preferred Page 12 of 53 Page 15 ▪ Remove part of the skull to allow brain to swell ▪ Bone flap placed in the abdomen ▪ Patient will need to wear helmet · Psychosocial Support o Patient , Family, Support, Information, Chaplain or social services Traumatic Brain Injury · Skull Fractures o Open vs Closed ▪ Cranium open and brain exposed or closed o Linear skull fracture ▪ Basilar skull fracture *** · Battles signs, raccoon’s eyes, CSF from nose and ears ottoreah or rhinorrhea (halo signs – blood in middle CSF outside) – take piece of gauze put drop on it and the CSF will go to the outside and blood in the middle. Never put an NG tube because you put it in the brain. o Depressed skull fracture o Comminuted skull fracture · Traumatic Brain Injury Classifications: o Primary ▪ Direct injury to brain · Coup/Contrecoup Injury (whiplash) ▪ Types · Concussion O Most common associated with TBI, does not show up on CT, rest the brain. Based on clinical treatment. Only tx: is to rest the brain. · Contusion: Bruise of the brain associated with leaking blood vessels. · Penetrating injuries: Ex: Gun shots Page 15 of 53 Page 16 · Diffuse axonal injuries: O Most severe, because the axons on neurons get torn or stretched (kind of like shaken baby syndrome) · Hematomas o Epidural ▪ Bleeding artery (medical emergency) ▪ Lose consciousness but quickly regain consciousness then date- rerate quickly Page 16 of 53 Page 17 o Subdural ▪ Bleeding veins ▪ Acute – loss of consciousness, worsening manifestations very quickly. ▪ Chronic subdural seen in the elderly o Intracerebral ▪ Bleeding of brain tissue itself ▪ Trauma or ruptured aneurism ▪ Complications of primary injury · Intracranial bleeding o Secondary ▪ Body’s response to the injury ▪ Consequence of initial trauma · Inflammatory response O Cerebral edema which increases ICP which leads to tissue hypoxia · Release of cytokines o Vasogenic edema · Loss of Autoregulation · Traumatic Brain Injury Management o Nursing (same as increased ICP) ▪ Neurological assessment · Glasgow Coma Scale ▪ Airway assessment ▪ ICP monitoring ▪ Hemodynamic monitoring Page 17 of 53 Page 20 · Ischemic Stroke o Large Artery Atherosclerosis – most common o Cardioembolic Events (A-fib) - most common o Small artery occlusion (Lacunar Stroke) o Cryptogenic – unknown cause. Looked at everything no cue reason. · TIA Page 20 of 53 Page 21 o Temporary symptoms then they go away Key*, indicator for stroke later. Do a full workup for patient. · Nursing Managements o Prevention: Most important. ▪ Public education regarding signs/symptoms ▪ Face, Arms(asymmetry), Speech, Time(tongue) “FAST” - sometimes tongue will devi- ate to left or right. o Assessment ▪ History is most important · Time of onset of symptoms for TPA O Time is important because 3-4 hours tape can be administered ▪ Neurological exam · Mental status, cranial nerve function, motor strength, sensory function, ne- elect, coordination ▪ NIH Stroke Scale (table 13-10) valuable tool to evaluate for a stroke, should be used nationwide · Universal, higher score the worse the patient ▪ Airway, breathing, circulation ▪ Hemorrhagic Variations · Localized or worst headache, nuchal rigidity, restlessness/irritability, photo- phobia, nausea and vomiting · Medical Managements o Hemorrhagic Stroke ▪ Goal: MAP < 130 systolic mm Hg (lower side) because you don’t want to increase bleeding. Ischemic patients we want the blood pressure a little higher, but not too high. Greater them 130. ▪ Glycemic management Page 21 of 53 Page 22 ▪ Diagnostic exams · CT evaluation · Laboratory tests ▪ Medications · IV antihypertensives · Manage ICP o Osmotic diuretics ▪ Monitoring for signs of vasospasm Page 22 of 53 Page 25 o Safety precautions/Seizure Precautions Ex: Pads, suction, 02, o Educate patients · Medical Management o Medications: Compliance in taking meds is important, no driving, knowing signs to identify. ▪ Benzodiazepines – drug of choice lorazapam ▪ Anticonvulsants · Dilantin – getting Dilantin level is important · Hereby ▪ Phenobarbital only as last result. CNS Infections - Bacterial Meningitis · A neurological emergency most concerned about · Infection of the pia and arachnoid layers and CSF · Transmission o Blood o CSF contamination during surgical procedures o Skull – direct openings to brain will put you at high risk for meningitis · Clinical Manifestations o Headache, Fever, Photophobia, Petechial Rash on trunk, Nuchal Rigidity – Signs of this: Brudzinski – lift head and knees flex – positive sign Karnack’s sign – flex him and knee and the pt. will feel pain and resistance when straighten leg and sometimes head will lift up (pose- tie) · Diagnostics o Lumbar puncture ▪ CSF will look Cloudy, Lab will fine low glucose because bacteria is eating glucose, high protein, WBCs · Management Page 25 of 53 Page 26 o Antibiotics, Corticosteroids, Droplet Precautions, Seizure Precautions, Monitor for Increased CP Spinal Cord Injury (SCI) · Causes o MVC’s, Falls, GSW, Sport Injuries, Diving Accidents · Primary versus Secondary Injury to the spinal cord o Primary is injury to spinal cord itself o Secondary is body’s response to spinal cord injury Page 26 of 53 Page 27 · Complete Lesion (injury to spinal cord is called lesion) o Total loss below the level of Injury o Movement, sensation, reflexes · Incomplete Lesion o Sparing of some function below the injury o Some function below injury – more common partial loss o Anterior Cord Syndrome o Central Cord Syndrome o Brown-Sequard Syndrome · Spinal Shock (or primary injury) o Complete loss below level of injury o This should resolve in maybe a few days or weeks o Resolves when sensation comes back ▪ Motor ▪ Sensory ▪ Reflex activity · Neurogenic Shock (or secondary injury) or system o Disruption of autonomic pathways o SNS shuts down and PNS takes over ▪ Temporary disruption of autonomic pathways below level of injury · Assessment o Airway and ventilation key – make sure we need to protect airway and patient is able to breathe. o KEY: Stabilize spine FIRST o Paralysis of diaphragm and intercostal muscles will result in ineffective breathing patterns ▪ C1 to C3: ventilator dependent Page 27 of 53 Page 30 · Medical Management o Spinal cord stabilization short term and long term. ▪ Halo vest ▪ Surgical intervention o Medication ▪ Glucocorticoids – high dose ▪ Vasopressors/fluids Page 30 of 53 Page 31 ▪ Proton pump inhibitors ▪ IV fluids · Thermal Burn o Fluid loss o 90% of cases Burns o Related to time of exposure to very hot or cold objects Ex: fire, stoves, hot eater o Severity of burn is the amount of time you are exposed to the cause. · Chemical injury o Cause protein denaturation (why they are so bad because of break down protein in our tis- sue) o Acids ▪ Cleaning products ▪ Acids stop burning once the agent is removed or flushed from the skin. ▪ You can wipe down the acid and break down of protein will stop. o Bases ▪ Worse than acids ▪ Ex: Oven cleaner ▪ Even after it is removed from skin tissue continues to break down o Organic compounds ▪ Most serious because cause deep tissue denaturation – get to deep layers of skin ▪ Organic compounds can deeply penetrate leading to internal injuries ▪ Ex: Gasoline · Electrical Burns/injury o Internal injury can cause dysrhythmias; you can see spinal cord injury because it could throw you. o Can cause lethal ventricular fibrillation, central nervous system defects and injuries and tetany causing respiratory paralysis. Page 31 of 53 Page 32 o Burns may not look severe on the outside because the current enters the skin and follows the path of least resistance. Therefore there is a lot of damage underneath the skin that may not be as visible. · Inhalation injuries o 20 to 50% of people who had a thermal o Occur after fires or chemical leaks in enclosed spaces. Systemic injury can occur due to toxic gas exposure such as carbon monoxide and cyanide poisoning. o Shallow breathing, pulmonary problems, stridor, o Clinical indications of injury ▪ Facial burns good chance they will have inhalation injury, presence of soot(hash) around mouth and nose, dark tinged sputum, respiratory difficulty o Intervention Page 32 of 53 Page 35 · Bur ns ▪ Arm - 9% each. 4.5 on front 4.5 on back ▪ Torso – 18% - chest 9% - abdomen 9% ▪ Back 18% - 9% upper back – 9% lower back ▪ Legs 18% front and back 9% ▪ Peri area – 1% ▪ Ex: Abdomen B legs = 18, abdomen 9. Lower back 9, front head 4.5 = 40.5 o Hypermetaboloic state b/c your body is trying to heal itself. o At risk for hypovolemic shock o Symptoms same for hypovolemic shock o Patients need a lot of calories to heal (high metabolic state) ▪ High protein · Burn Treatment o Parkland Formula: 4mL x kg(ideal) x TBSA that pt. has been burned – this is how we give fluid back. Ex: 4 mL x 86 x 40 = 13,760 total you will divide by 2 = 6,608mL total you dived in half and the first total you will give in first 8 hours the patient was burned. First 8 hrs. = 860ml/hr. of fluid… the sec- on half of your original total you will give in the first 16 hours. You will set the pump at 430 mills ON EXAM KNOW THIS Ex: 4 m: x 60 x 70 = 16800 … first 8,400... 1040 ml/her first then 525 ml/hr o Resuscitative phase · Within the first 48 hours after the burn ▪ Airway · Early intubation ▪ Breathing · 100% humidified oxygen via face mask or through mechanical ventilation for CO poisoning. ▪ Circulation · Fluid resuscitation using the Parkland Formula · Cardiac monitoring—especially for electrical burns · Patients will still require maintenance fluid that matches urine output. ▪ Neurological Status · Changes in neurological status may indicate potential complications such as seep- sis, hypoxemia, or hypoperfusion ▪ Renal status Page 35 of 53 Page 36 · Intake and Outtake ▪ GI system · Monitor for ileus or Curling’s ulcer - monitor for stress ulcers and contuse stress ulcer prophylaxis · NGT insertion · Monitor for intraabdominal hypertension (life threatening complication) ▪ Integument system · Main focus is prevention of infection and sepsis · Wound assessments · Tetanus immunization · Prevent hypothermia ▪ Monitor blood and electrolytes · Refer to the Laboratory Alert Table on page 640. ▪ Replace patients fluids Page 36 of 53 Page 37 · Parkland Formula o 4ml x kg x % of body burned o Split total in half ▪ First half is given in the first 8 hours ▪ Second half is given over 16 hours · Isotonic fluids – probably lactate ringers o Acute Phase 2nd phase ▪ 48-72 hours after burn- until burn is closed ▪ This phase can last months. ▪ Begins when patient starts to dieresis ▪ Continue interventions of resuscitative phase ▪ 2 greatest concerns · Pain – very painful o IV narcotics o PCA – if alert and aware this is preferred so they can control their pain. · Infection – number 1, huge risk o No skin to protect them ▪ Goes until wound is closed, can last weeks to months. o Rehabilitation Phase ▪ Getting patient as close to function as possible. ▪ Focused Therapy: PT, OT, and social work. A lot of support. ▪ Takes weeks to months o Wound care ▪ Debridement (deep partial and full thickness) ▪ The type of burn will tell the extent and care of the wound. ▪ Removal of old and dead skin with a brush or scrubber. Very painful ▪ Xenografts - pig (animal skins) ▪ Autografts – own skin (self) ▪ Synthetic graft ▪ Allografts – cadavers or someone else ▪ Compartment syndrome in wounds that go all the way around arms and legs, or in the abdomen. 6 Ps · Escharotomy to relieve pressure o Concern: Circumferential burns and compartment syndrome from Page 37 of 53 Page 40 Interventions Nursing Monitor I/O, daily weights, BUN, creatinine. Infection pre- venation, delaying progression by monitoring peak and trough levels and dosage adjustments. Page 40 of 53 Page 41 Medical Prerenal—correct hypovolemia, positive inotropic agents for decreased cardiac output and treat underlying cause. Intrarenal—drug therapy, protein and electrolyte restrict- ton, removal of toxic agents. Postrenal—remove the obstruction Treat the cause: Ex: Get perfusion back to kidneys If post renal get rid out of obstruction. Ex: Kidney Pharmacological Diuretics are controversial and it depends on the cause of the failure and can be used to manage fluid overload Dopamine—also controversial – vasoconstriction, vase- presser N-Acetyl cysteine (Mucomyst)—used for patients who are at risk for contrast induced kidney injury. Dose before and after. Give before and after giving contrast dye – it the smelliest! Dosage adjustments Dietary The goal is to provide enough nutrients to maintain homeostasis. Sodium and potassium restrictions. Fluid restriction Hyperkalemia— associated with diastole. Can cause ECG changes that begin with tall peaked T-waves , Potassium restriction. Dialysis and Kayexalate are the only therapies to reduce potassium levels. Administrate- ton of Kayexalate requires bowel function (bowel sounds). You can give kay rectally. Page 41 of 53 Page 42 progressing to a wide QRS complex, flat- toned p wave, to ventricular tachycardia, ventricular fibril- lotion and then cardiac stand- still. Insulin, albuterol and sodium bicarbonate will temporarily push potassium back into the cell. Calcium gluconate will protect the heart from the effects of elevated serum potassium, it doesn’t do anything to potassium it just protects the heart. If giving insulin give them food/glucose otherwise you will bottom out blood sugar. Potassium is associated with diastole in heart, as potash- sum gets higher it will cause slowing down of heart. Dialysis - if meds do not work you will need this Continuous Renal Replacement Therapy (CRRT) Hemodialysis Peritoneal dialysis (rare) · Dialysis o Vascular access ▪ Catheters · Short term – has arterial port or venous port · Do not touch the catheter! Assess it and nothing else. Assess site make sure its intact. Strictly for dialysis. ▪ Fistula or Graft · Long term Page 42 of 53 Page 45 Peritoneal dialysis—A dialysate solution is admonish- tired into a peritoneal catheter and “dwells” for 4-6 hours. The peritoneum acts as a semipermeable mem- brane to allow for shifts of waste products out of the blood stream into the peril- tone that acts as a riser- void. The waste is drained aft- term 4- 6 hours. After the fluid is drained, more dialysate is administered into the peril- tonal catheter. Does not clean out your blood as good. Aseptic technique, assess for cloudiness of the peril- tonal drainage, warm the fluid to prevent cramping. Have the patient turn if fluid is not draining and check the catheter pa- teensy. Do not give BP meds before dialysis Catheter perforation of the peritoneum, catheter block- age, cramping if the fluid is too cool, patient discomfort, peritonitis, metabolic disturb- bancs, hypovolemic. Peril- otitis (monitor fluid coming out of the patient) Risk for peritonitis since di- recto access to abdomen, Fluid out should be clear if fluid is cloudy it prob is peritonitis. GI Upper GI Bleeding Causes: · Peptic Ulcer Disease (smoking, H. pylori, NSAID use, Alcohol, etc) Page 45 of 53 Page 46 · Stress Ulcers · Mallory-Weiss Tear – when you vomit a lot, longitudinal tear of the esophagus. We see this with free- quant episodes of forceful vomiting. This is why we see this with people who binge drink. Depending on the severity we will let this heal on own or pt. might need surgery. · Esophageal Varices – complication of cirrhosis Clinical Manifestations: Depend where the blood come from. · Vomiting/NG drainage of blood or coffee ground emesis. – a sign of old blood. · Melena—black tarry stools which indicate digested blood from the upper GI tract · Hematochezia (bright red blood)—usually seen in lower GI bleed but can be seen in a massive upper GI bleed · Signs and Symptoms of hypovolemia (hypovolemic shock) · Abdominal discomfort Diagnostics: · CBC, coagulation studies, electrolytes, LFTs, ABGs · Endoscopy and barium study – diagnose and treat at the same time test of choice. Page 46 of 53 Page 47 Management: · Airway management (vomiting and risk for aspiration) The biggest concern is AIRWAY. If they are vomiting there is a chance you can aspirate. If you are losing a lot of blood it can affect LOC, then you cannot protect your airway. Other Concern is risk for hypovolemic shock. – Massive blood loss. · Supplemental oxygen · Hemodynamic stabilization · Gastric lavage — to provide visualization of the fundus right before en endoscopy, Pt. must have ng tube. Instill 1-2L of room temp saline in to the patients NG tube. Remove with suction or gravity. Continue to do this until what you are getting out is clear. Medications · Proton pump inhibitors · Antibiotics if the cause is H. pylori Endoscopic therapies · Sclerotherapy – inject schlerotptic agent · Thermal therapy · Banding of esophageal varices · Antibiotics if patient has h.pyloti. · Maintenance of airway and breathing is extremely important during endoscopy Surgical Therapies (last resort) NOT GONNA TALK ABOUT · Indicated for patients who continue to bleed despite endoscopic therapies or for perforations · Antrectomy · Gastrectomy · Gastroeneterectomy · Vagotomy · Bill Roth I · Bill Roth II Treatment of Variceal Bleeding · Somatostatin or octreotide Vasoconstricts blood vessels in GI tract to decrease splanchnic blood flow and lower portal pressure · Vasopressin lowers portal pressure. Patients usually receive nitroglycerin to maintain coronary artery perfusion. Does the same thing as somatostain – but it constricts all of your vessels. So watch out for blood pressure. · Sclerotherapy · Trans jugular Intrahepatic Porto systemic Shunt (TIPS) –placed in the liver so blood does not back up into the esophageal vein · Esophogastric Tamponade (Airway management is a high priority) – NG with a balloon on it. Page 47 of 53 Page 50 o Diagnostic tests ▪ Elevated liver enzymes (ALT, AST), not specific to cirrhosis though ▪ Specific labs to look for Elevated bilirubin and elevated ammonia levels (true signs/true labs that patient has cirrhosis) ▪ Changes in coagulation studies o Treatment ▪ Supportive ▪ Treat complications – you need a liver transplant but can treat the complications ▪ Ascites (liver can’t make albumin) respiratory problems. Page 50 of 53 Page 51 · Maintaining respiratory support because ascites can put pressure on the di- ashram · Bed rest · Low sodium diet and fluid restriction · Diuretics · Paracentesis Monitor vital signs (albumin may need to be admonish- tired post procedure), make sure the patient is NPO and the bladder is empty), also monitor for peritonitis. Give patients albumin. Make sure patient pees first or it can rupture bladder. This is more than one time. Aft- term this you should give them some albumin. · Peritoneovenous shunting · TIPS procedure o Hepatic Encephalopathy ▪ Occurs because the liver cannot convert ammonia to urea. Ammonia comes from the breakdown of protein. Liver cannot filter out ammonia so LOC changes. ▪ HE is characterized by mental status changes and asterixis (hand flap- ping tremor). Hold out hands and if they have asteroid one hand will flap. ▪ Can be precipitated by conditions such as infection, GI bleed, blood transfer- sons, analgesics, TIPS procedure. · Lactulose (1st choice) – poop it out – it will pull the ammonia and out it out. · Metronidazole · Neomycin · Provide a safe environment o Hepatorenal Syndrome—not well understood but the kidneys begin to fail due to poor perfusion pre-renal injury ▪ Renal replacement therapies o Hepatopulmonary Syndrome—hypoxia ▪ Oxygen ▪ TIPS ▪ Liver transplantation · Endocrine o Type 1 – insulin dependent. DKA is a risk. o Type 2 risk for developing HHS. o Job of insulin puts glucose back in to cells. o Hypoglycemia ▪ Too much insulin or took it and didn’t eat ▪ CM · Changes in LOC, shakiness, dizziness, sweaty, ▪ Treatment Page 51 of 53 Page 52 · They can eat: sugar and carbs. Give them juice and crackers. · Can’t eat or drink give glucagon or D50 (preferred) o Hyperglycemia ▪ DKA · Common in type 1 · Has KETONES · CM: O Ketones in urine, kussmaul respiration, fruity breath, acidic – metabolic acidosis because they are trying to compensate. Hyperglycemia, fluid Page 52 of 53