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SCORE School Organ System Dysfunction, Part 3
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SCORE School Organ System Dysfunction, Part 3
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Segment:0 .
AMIT JOSHI: Hi, everyone. It's Amit Joshi from SCORE. Welcome to SCORE School. This week, we're going to be covering organ system dysfunction, the third part of three. I'm really delighted to be introducing Dr. Susan Kartiko. She is an assistant professor of surgery at the George Washington University School of Medicine. She earned her M.D. and PhD from Texas A&M Health Science Center in Texas, then did a surgical residency at Einstein Healthcare in Philadelphia, followed by a surgical critical care fellowship at Boston University.
AMIT JOSHI: After three years at the University of Massachusetts Bay State in the division of trauma, emergency surgery, and surgical critical care, Dr. Kartiko moved to Washington, DC, where she's now at GW. Her research interests include surgical education, trauma surgery, and geriatric trauma. She's going to be covering the modules of neurologic dysfunction, pain agitation and delirium, and hepatic failure and hepatorenal syndrome.
AMIT JOSHI: Dr. Kartiko, thank you so much for joining us, and go ahead.
SUSAN KARTIKO: Thank you for having us and a warm welcome. Today we will be talking about organ dysfunction part 3, and this is the QR code to log in for your attendance. The topic that we'll be talking about today will be neurological dysfunction both trauma and non-trauma, pain delirium and agitation, and lastly, hepatic failure and hepatorenal syndrome. First, we're going to start with the neurological dysfunction.
SUSAN KARTIKO: Many surgical patient presents with neurological dysfunction, and this comes from altered mental status due to many different causes. Most common causes could be sepsis, could be from traumatic brain injury, could be from delirium, could be from spinal cord injury, et cetera. As the surgeon, we will have patients with neurological dysfunction, so we need to be able to recognize, diagnose, and intervene on neurological dysfunctions in our patients.
SUSAN KARTIKO: So first we'll discuss about neurological dysfunction in trauma patients. As usual, all patients who arrive as a trauma will need to be assessed in a systematic way. In the US and many places in the world, we use ATLS for this. ATLS dictates that all patients that come into the trauma bay needs to be assessed ABCDE-- airway with a C-spine immobilization, B for breathing, C for circulation, and then D for disability.
SUSAN KARTIKO: And this is the time that we assess our patient's neurological dysfunction, or if there is one. We usually do this by using the Glasgow Coma Scale, and all patients who have GCS less than 8 will need to have their airway protected. And then ATLS dictate that we look into the environment, such as the temperature they're in, and to expose them.
SUSAN KARTIKO: The Glasgow Coma Scale is a scale to assess a patient's level of consciousness in head trauma. Patient's GCS should be done after the patient is hemodynamically stable, or as stable as can be, and preferably not when they're on sedatives. GCS looks into three different criteria-- the eye opening, the verbal response, and motor response. Eye opening has a scale from 1 to 4, as you can see on the table.
SUSAN KARTIKO: Verbal response has a scale from 1 to 5, and motor response has a scale from 1 to 6. The lowest GCS a person can have is 3, and the highest is 15. When we determine for patient's GCS, we obtain the highest score the patient can score, also knowing that GCS can change, and it may fluctuate during a certain time. Again, with patients who have a GCS less than 8, airway protection is important, and it's to be secured.
SUSAN KARTIKO: Trauma patients who arrive with a low GCS, it could be due to many different things. So the differential diagnosis could include traumatic brain injury. However, that's not the only cause that patient may have for a neurological dysfunction in a trauma situation. End organ dysfunction, such as due to hemorrhagic shock, can also cause low GCS.
SUSAN KARTIKO: Spinal injuries should be entertained, especially if the patient is awake; however, they're not able to do the motor portion of the scale. It could also be due to drugs or medication overdose. It could be due to seizure. [? Many ?] [? aphasic ?] people have [? ICP ?] and had a seizure and that their alertness is affected. It could be that they have a seizure disorder, and that's why they're having the seizure, and when-- got into a traumatic situation, such as motor vehicle crash.
SUSAN KARTIKO: And it could be due to many different things. The neuro exam on a trauma patient would be focused on signs of trauma, especially in the head or in the spine. We should also look into pupillary exam, gross motor and sensation exam of the patient. While running the trauma, be aware of patient's vital signs, which may be showing signs of brain stem herniation, and this is called Cushing response.
SUSAN KARTIKO: Cushing response is the physiologic response to acute elevation of the intracranial pressure. The hallmark is systolic hypertension and bradycardia, and this can be accompanied by irregular respiration pattern. To prevent further elevation of the intracranial pressure, especially in the trauma bay, there are several things that can be done. If the patient is already intubated, then we can hyperventilate them through the vent.
SUSAN KARTIKO: This is only a transient response, should not be used for a prolonged effort to keep someone's ICP low. And the goal for the hyperventilation is for pCO2 between 30 and 35 millimeter mercury. It should not be any lower than that. The other thing that we can give is hyperosmolar therapy, such as hypertonic saline and mannitol. If the patient blood pressure is good enough, then we should give the patient sedation and pain control, such as opioids, and sedation can be the form of Precedex, in the form of propofol, depending on whether the patient is intubated or not.
AMIT JOSHI: Dr. Kartiko, could I ask you one question there? So a common at least multiple choice question is to prioritize those three-- hyperventilation and the hyperosmolar therapy and sedation pain control. So how would you actually put them in order of intervention?
SUSAN KARTIKO: So if the patient is intubated, the fastest way to decrease someone's ICP is via hyperventilation. But this is only to buy time for a little bit, so that we can have the hypertonic saline ready, make sure the patient has an IV, that it's secure. And then the next thing that I would use is actually hyperosmolar therapy. Sedation and pain control is also important, but sometimes these are not necessarily possible to be given if the patient has other like low blood pressure or other hemorrhagic signs.
SUSAN KARTIKO: And pain control can be given judiciously, but sedation may not be the one that we want to use, especially if the patient's GCS is already low.
AMIT JOSHI: Got it. Thank you.
SUSAN KARTIKO: When we are discussing about elevation of the intracranial pressure in trauma patients, we should understand the Monro-Kellie Doctrine The Monro-Kellie Doctrine explains the relationship of cerebrospinal fluid, blood in the brain, volume, and pressure when there is an increase in mass. This increase in mass can be in the form of tumor or blood. Intracranial pressure is unique, due to the skull preventing expansion in the event of increased intracranial mass.
SUSAN KARTIKO: When there is a new mass-- for example, blood-- the system displaces CSF and blood first, and thus there is a compensation of the volume increase to maintain a certain pressure. You can see this actually in the graph of the volume pressure curve. There is still a flat portion of the pressure graph. At a certain point, however, the system will seek to compensate, and with a small increase in mass, the pressure can increase in an exponential manner.
SUSAN KARTIKO: This is why after a certain point an increase in intracranial bleed, even by a small volume, can increase the risk of herniation very rapidly. So how do we diagnose and treat TBI? Diagnosis for traumatic brain injury-- the CT scan is the gold standard. Once TBI is diagnosed, the next thing that we do is neuro checks to determine if there is a neurological dysfunction that is worsening.
SUSAN KARTIKO: Neurosurgical intervention should be considered. However, if surgery is not indicated, prevention of secondary insult of patient's brain should be the goal. Traumatic brain injury can be categorized into two type of insults. One is the initial insult to the brain, which is the initial injury, and then the second one is a secondary insult. Patient with TBI that was for secondary insult. The secondary insult can come from extracranial sources and intracranial hypertension.
SUSAN KARTIKO: The intracranial sources can be from hypoxia, hypotension, fever. However, this whole thing as a secondary insult can worsen the outcome of TBI, much worse than the primary insult. To prevent secondary insult in TBI, we need to prevent intracranial hypertension and avoid extracranial things, such as hypotension, hypoxemia, hyperthermia or fever, and seizure.
SUSAN KARTIKO: So first we'll look into how to maintain a low ICP. The easiest thing to do, especially after a spinal cord injury is ruled out in a trauma patient, is to elevate the head of bed to 35 to 45 degree. ICP monitor can be used, especially if patient's GCS is less than 8, and neuro exam is no longer very good at that point, because the patient is comatose. Once the ICP monitor is inserted, the goal is to maintain a cerebral perfusion pressure, which is CPP.
SUSAN KARTIKO: CPP is obtained by MAP minus ICP, and we want to maintain the CPP between 60 and 70 millimeter mercury. To do this, there are two things that you can do technically. The first one is to increase the MAP, and the second one is to decrease the ICP. We typically try to decrease the ICP, especially if the MAP is already normal. If it is hypotensive, then the next thing that we need to do is maybe if it's due to hemorrhagic shock, then to give blood and to make sure that we can stop the bleed.
SUSAN KARTIKO: However, to decrease the ICP, we can do many things, and this is expanded from what we could do in the trauma bay because at this point we have imaging, and we know exactly what is wrong with the patient or presumably. So the things that we can do again is hyperosmolar therapy. We certainly can give sedation at this point, because we already know what kind of injury the patient has. Pain control becomes important as well.
SUSAN KARTIKO: If hyperosmolar therapy, sedation, and pain control is no longer able to decrease the ICP, we can venture into paralytic. However there's still-- we still need to reassess for surgical intervention. Maybe patients who didn't need to have surgery done prior, now becomes more imminent to have some sort of surgical intervention. The surgical intervention that can be done is decompressive craniotomy, which has been shown to reduce ICP and may improve outcome.
SUSAN KARTIKO: However, studies have shown that bifrontal decompressive craniotomy, while reduces ICP and ICU length of stay, has not really improved outcome. This is the MAP, the ICP part. Then the next part would be to manage the extracranial problems, including hypoxia. The goal for our patient is to prevent secondary insult is not to crank up the oxygen as high as we can but to maintain a normal paO2.
SUSAN KARTIKO: The other thing that we need to do is avoid fever, and the goal is not hypothermia but normal temperature. We also need to avoid seizure. That's why these patients are given anti-seizure prophylactically. We also need to maintain their nutritional requirement, and ASPEN guideline has said to feed the patient with TBIs within 48 hours of admission. Chlorhexidine oral care is to prevent a pneumonia.
SUSAN KARTIKO: Pneumonia of course causes hypoxia, may cause hypotension, may also cause a fever, all of which are not good for a patient with TBI. There is no role for steroids for traumatic brain injury. And the other thing that we need to do is avoid hypotonic solution to prevent cerebral edema. That means no LR, that normal saline. It's usually the one that we use for people with TBI.
SUSAN KARTIKO: The prognosis of traumatic brain injury has been studied quite extensively. There are certain things that we know, such as low initial GCS, usually confers to a worse prognosis. Increase in age is a strong independent risk factor for worse prognosis as well in TBI, and the significant increase in poor outcome for patients above 60 years old. Based on the CT scan itself, there are certain things that can determine prognostication.
SUSAN KARTIKO: We know that an abnormal CT scan in 90% of patients-- we know that there is about 90-- abnormal CT scan in 90% of patients with severe head injury. However, the absence of CT scan abnormality does not really preclude high ICP and that new lesion may develop in 40% of the patients. The other features in CT scan that confer to worse prognosis is compressed or absence of the basal cistern.
SUSAN KARTIKO: This indicates three times risk of high ICP, which of course is related to outcome. Traumatic subarachnoid hemorrhage is a worse prognosis, and it confers to two times mortality to other type of TBI. And of course midline shift confers to worse outcome as well, because that shows an increase in intracranial pressure due to MAP.
SUSAN KARTIKO: In trauma patients with concerns of spinal cord injury, the symptoms usually decrease in gross sensation or motor function in the extremities. And this can also cause tingling or decrease in sensation in their fingers or toes. Inline immobilization is very important, especially in the beginning part of the workup in the trauma bay. The spinal cord injury, the imaging that we usually get is the CT scan, usually C-spine, thoracic, and lumbar, and then MRI when there is a spinal cord injury that is suspected.
SUSAN KARTIKO: The goal of the spinal cord injury treatment is to maintain spinal cord perfusion with surgical intervention if needed. Steroid has not been shown to be beneficial in the transection injury of the spinal cord, but it could be beneficial for people who have central cord syndrome. So central cord syndrome patient in trauma, it could be that they are already narrow. They have a spinal stenosis, and the trauma causes injury, and they present as central cord syndrome patients.
SUSAN KARTIKO: Sorry, my computer just went kaput. I need to open the PowerPoint again. Sorry.
AMIT JOSHI: OK.
SUSAN KARTIKO: And then [? it ?] [? starts. ?] OK. All right now, let's discuss neurological dysfunction that is not due to trauma nor TBI. So we encounter patients with neuro-disturbances sometimes, and this can be due to many things, and we find them on the floor. And this patient usually presents with altered mental status. And this altered mental status can be due to many different things, such as end organ hypoperfusion, maybe due to hemorrhagic shock, maybe due to septic shock, maybe due to cardiogenic shock.
SUSAN KARTIKO: Other things that can cause neurological dysfunction in a surgical patient includes physiologic derangement, such as high ammonia in people who have liver failure or uremia in people who have kidney failure. Primary infection of the brain, such as meningitis and infectious encephalopathy, can also happen. Seizure can also be a cause of neurological dysfunction of surgical patients. Delirium/agitation is another cause.
SUSAN KARTIKO: And last but not least is a stroke. Patient may also have stroke, and if that's the case, then of course care needs to be done pretty quickly to render better outcome, especially for a stroke patient. For the treatment for all these patients who have altered mental status or neurologic dysfunction that are not due of trauma, the first thing that we need to do is stabilize the patient.
SUSAN KARTIKO: We can use the same mnemonic of ABC-- maintaining airway, breathing, circulation. If the mental status is bad enough, then if certain airway needs to be done, such as intubation, we should do that. And then we need to move on to diagnosing by going through the workup, looking at labs, looking at chest X-ray, looking at EKG, CT head if it's needed. And of course, we need treat the underlying cause.
SUSAN KARTIKO: So that's the end of the neurological dysfunction part of the module. This is again the QR code to login in--
AMIT JOSHI: [INAUDIBLE]. Thank you. I'll just re-emphasize the point you made, which is how important the intensivist or the surgeon managing the global status of the patient can be in treating neurologic dysfunction. So it's something I know that our critical care faculty always emphasize in the unit, but this is why critical care is such an important part of surgery.
AMIT JOSHI: The neurosurgeons may be managing the brain or the spine. The orthopedists might be managing the extremity injuries, but we are still responsible for maintaining the organism as a whole. And so that was a nice review of avoidance of secondary injury in particular. Thank you.
SUSAN KARTIKO: Thank you, and I couldn't agree more with the sentiment. OK, so the next topic we'll be talking about is pain, agitation, and delirium. The first thing I'll be talking about is pathophysiology of surgical pain. Pain is due to nocioceptive activation via the prostaglandins, interleukins, cytokines, and neurotrophins. In injury, the decrease in tissue pH, oxygen tension, increase in lactic acid, along with an increase in peripheral granulocytes can cause pain at rest and increased response to stimuli at the site of injury.
SUSAN KARTIKO: And this is the primary hyperalgesia. Central sensitization can in turn amplify the noxious input during and after the surgery. To assess for pain, we should ask our patients the location of the pain. Patient comes in with a certain pain, pain in the belly, pain in the leg, and we should assess them. What is the location of the pain, the duration of the pain, the quality of the pain, and what makes it better or worse, and then the intensity of the pain.
SUSAN KARTIKO: Quality of pain can be divided into somatic, visceral, and neuropathic pain. Somatic pains are usually dull and aching. They are usually well localized, and these are the pains that are caused by bone fracture, bone mets, muscle strain. So there is a localized area where [? they're ?] [? saying, ?] the area that may be injured. Visceral pain-- it could be dull or sharp.
SUSAN KARTIKO: It could be collicky, comes and goes. It could be well localized or it could be referred. And these are more of the gastritis pain, gallstone pain, pancreatitis pain. Then there is neuropathic pain. This is more a burning sensation, lancinating, itching sensation. And it usually follows the path of the nerve, and this can be from herpes zoster type of pain, spinal disk pain, diabetes pain, such as diabetic neuropathy.
SUSAN KARTIKO: The intensity of pain is usually communicated in a scale. The most common scale is American scale from 0 to 10. Usually we say what is the worst pain that you can have, and that would be 10. And be careful with that, because people may not have had pain. And so we usually say things like, if you can imagine yourself being hit by a truck, that would be number 10.
SUSAN KARTIKO: Or if you've given birth before vaginally, that would be number 10. And then we also ask during our interview what kind of treatment the patient has tried. Oh, I take Tylenol, doc. Or I take ibuprofen or I put warm compresses. Does that work at all? The last thing, and usually we kind of skip it in our patient, is that the impact of pain on life, whether the pain is affecting the activity of daily living.
SUSAN KARTIKO: Does it affect your sleep? Does it wake you up from sleep? Does it affect your eating? Does the pain make you not want to eat at all? Does it affect how you move? Do you move in a certain way now because your hip is bothering you, or your back is bothering you. And then lastly, that it's more important to our patient is whether the pain affects their daily working life.
SUSAN KARTIKO: The management of pain, especially for surgical pain, should start during the pre-op time. This includes setting expectations for the pain after the surgery. Pain management should not be an afterthought. Additionally, pain management should depend on the type of surgery that is being performed and the setting i.e. emergency surgery or urgent surgery may have more pain associated with it compared to elective.
SUSAN KARTIKO: The type of surgery being performed, if it's a laparoscopic type of surgery versus open surgery. The expectation of pain should be given prior to the actual surgery. To control pain, it is recommended that we use multimodal pain control, meaning utilizing medication that target different receptors and using different modalities, such as blocks to minimize the use of opioids.
SUSAN KARTIKO: Of course, nowadays we have the opioid epidemic, and all efforts should be done to decrease that, and that we use many different things to control pain. The different kinds of medication that can be used to alleviate pain include Tylenol or acetaminophen; NSAIDs, such as ibuprofen and Celebrex. We can use muscle relaxant antineuropathic pain medications as gabapentin, and of course opioid.
SUSAN KARTIKO: Pain should be viewed as a continuous thing with peaks and valleys, so pain needs to be assessed routinely, and pain medication administration needs to be adjusted depending on the pain that the patient is having. Just because it's usual for a surgical patient to have oxy 5 every 5 to 6 hours, that does not mean that works for everybody. It also does not mean that that alone should be able to treat all the peaks and valleys, so we have to arrange our pain medication administration based on the pain that the patient is feeling at the time.
SUSAN KARTIKO: Pain is very important to be controlled appropriately to avoid delirium and agitation and allow for appropriate recovery from surgery or injury. This is a table of different pain control modalities. If you look at the first column, there is a different technique, and the first technique is neuroaxial opioid analgesia. This is more into the epidural and spinal anesthesia routes, and we can administer opioids through it along with local anesthetic.
SUSAN KARTIKO: So the common medication we use in there would be the fentanyl in the epidural or maybe even dilaudid or morphine. And this has been shown to improve pain relief compared to pre-incisional, oral, or IV or intramuscular administration, so it is quite good to use for a certain type of operation. The next one that we can use is peripheral or central regional analgesia or blocks.
SUSAN KARTIKO: We're talking about intercostal blocks for rib fracture, plexus blocks, local anesthetic infiltration or in the incision, when we're making incision. And the common medication we use is bupivicaine, ropivicaine. It could also be lidocaine if it's for the local anesthetic. And the purpose of this is to reduce inflammation, alleviate pain, and reduce analgesic requirement later on including opioid. It has been shown to reduce length of stay, especially for rib fracture, and improve recovery time.
SUSAN KARTIKO: Next medication is non-opioid analgesic. We talked about it briefly before. Acetaminophen, NSAID, antidepressant, alpha-2 agonist, anticonvulsant such as gabapentin, and NMDA receptor, which is ketamine that can be given as IV medication either drip or as boluses. And lidocaine, which can also be given as drip or boluses. And this is all done to reduce the opioid requirement.
SUSAN KARTIKO: The next one is the parenteral analgesic, which is the IV opioid. And we have morphine, fentanyl, dilaudid, sufentanil. It is important to use the lowest dose possible for this, as well for the oral opioid analgesic, which includes oxycodone, tramadol, hydrocodone, morphine, and dilaudid. And these can also be paired with acetaminophen in the form of Percocet and Vicodin.
SUSAN KARTIKO: All right, so that would be the portion for the pain. Next we're going to talk about agitation and delirium. Delirium itself is a disturbance of consciousness. It is marked with inattention, accompanied by a change in cognition or perceptual disturbance. So they can have some hallucination that develop over a short period of time. So hours, days, and fluctuates over time.
SUSAN KARTIKO: The etiology of this multifactorial there are thoughts that some people who already have anatomic deficits are more prone to it. And then the other thing that could be the cause of delirium is neurotransmitter abnormalities. And this could be in the form of derangement in level of serotonin, acetylcholine, dopamine, or other neurotransmitter. And this can be due to systemic disease, toxic agents, withdrawal, such as withdrawal from alcohol, withdrawal from benzo, hypoxia, metabolic disturbances, psychoactive, and pain medication.
SUSAN KARTIKO: The outcome of delirium is the one that makes it a very important part for us to understand. Patients who have delirium have increased ventilator days, ICU days, and hospital length of stay, which all translates to increased costs for the patients and also for the health care in general. It is also associated with higher mortality both in hospital and after discharge. Patients who develop delirium also have a greater long term cognitive dysfunction, which is devastating for the patient.
SUSAN KARTIKO: To prevent delirium, we need to recognize the risk factor and focus our effort in modifying these risk factors, because the best way to treat delirium is prevention. So once we know the risk factor, we can modify these and hopefully prevent delirium from setting in at all. So the risk factor can be-- the mnemonic is I CAN STOP A DELIRIUM.
SUSAN KARTIKO: But as we go through this, it will make sense more than trying to memorize from a mnemonic. So the first one is impairment in ADL function, sleep and hearing or vision or sensory. This is basically everybody who is admitted to the hospital, because we always prevent them from getting out of bed, maybe, because we don't want them to fall. We certainly don't want them take a shower on their own. They have to always call the nurse.
SUSAN KARTIKO: Sometimes they couldn't even go to the bathroom on their own. Their sleep is disturbed because they're not in their own bed or in their own house. Sometimes a hearing aid is not working, or it needs more battery that nobody can change for them. And sometimes their glasses are lost, and all these can increase the risk of delirium. The other thing that makes it a risk factor is the patient already has some CNS pathology, such as stroke prior, such as having dementia or depression.
SUSAN KARTIKO: Or if they have multiple comorbidities, such as hypertension, diabetes, hyperlipidemia, anxiety, depression. All that combined can increase their risk of delirium. Alcohol and drug withdrawal is a big risk factor for delirium. Older age is also a risk factor, especially over 70 years old. New tethers, such as restraints, Foley catheter, IV fluid, NG tube, telemetry cables, can increase risk for delirium.
SUSAN KARTIKO: Surgery is an independent risk factor for deliriums, as well as trauma. Toxins is another one. Opioid use is a risk factor for delirium. However, uncontrolled pain is also a risk factor for delirium. Polypharmacies, especially for patients who are on benzodiazepine, anticholinergics, antihistamine, antipsychotic.
SUSAN KARTIKO: Anesthesia in general can increase delirium, risk for delirium. Deficiency in vitamins, especially B12, folate, and niacin. Exposure to drugs, especially psychotropic drugs. Hyper or hypothyroidism. Environmental changes. Low PO2 states, such as people who had a heart attack, or people who had PE, hypoxia from pneumonia, or having anemia.
SUSAN KARTIKO: Acute or chronic infection can cause delirium. Retention of urine or feces can cause delirium. ICU admission and institutional residences can increase delirium. Undernutrition or dehydration can increase the risk of delirium. And lastly, metabolic derangement of any kind. So there's quite a bit of risk factor, but these are all modifiable if we go through them one by one.
SUSAN KARTIKO: There are three types of delirium. Hyperactive, which is the one that we are very familiar with. A patient usually is restless and agitated, and/or agitated. And then there's hypoactive delirium, where patients are lethargic and apathetic. This is actually more associated with a higher mortality, because usually they are underdiagnosed. And then the third type is mixed delirium, where the patient has periods of both hyperactivity and hypoactivity.
SUSAN KARTIKO: To diagnose delirium, we can do a screening on our patient using CAM-ICU or bCAM for patients with a [? 4. ?] Both CAM-ICU and bCAM are pretty similar in that it is divided into four parts. And first we need to assess if the confusion is acute, unless it's on or off. If the patient has a stable baseline confusion all the time, he or she may have dementia and not really actually delirium.
SUSAN KARTIKO: So if it's yes, then we go to the second question. The second question measures for inattention. The test asks for the patient to squeeze or touch their hands when the toucher says the letter A in the sequence of letter, as you can see there, SAVEAHAART or CASABLANCA, and see how many times that there is error in that. If there's only zero to two errors, then the patient does not have delirium. However if there are more than two errors, then we move on to the next stage.
SUSAN KARTIKO: This part we want to measure-- we want to check the level of consciousness. If the patient-- and we do that using the RASS score. If the RASS score is other than zero, we can stop the test, and we can say that the delirium is present. If the RASS is zero, then we move on to disorganized thinking check and ask the questions, such as will a stone float on water? Are there fish in the sea?
SUSAN KARTIKO: Does one pound weigh more than two? Can you use a hammer to pound a nail? And if the patient has errors, there are more than one, then we can say that the patient has delirium. As I said, prior treatment for delirium, that prevention is best. And for this to happen, we need to have an interdisciplinary approach from the nursing staff, the nursing aide, geriatrician, the surgical team, the phlebotomist, the pharmacist, and most importantly, it's the family.
SUSAN KARTIKO: Nowadays it's difficult with COVID-19, but before that and hopefully after COVID-19, we try to incorporate family into taking care of the patient, and this helps tremendously to establish normalcy in their lives, so that they do not develop delirium. We also need to recognize and treat the precipitating factors and avoid medication that can worsen delirium. And this we can do by maintaining day and day/night cycles, opening their windows, turning on the TV or noise or radio during the day, and turning off TV and turning off the radio at night so they can sleep.
SUSAN KARTIKO: We want to minimize tethers. You want to avoid infection, meaning Foley. We can take out Foley as soon as that is indicated and not one day more. Pharmacological management of delirium is not really supported by strong evidence. In particular, benzodiazepines should not be used to treat agitation at all, because they can increase delirium.
SUSAN KARTIKO: The only exception to this is when the patient has delirium tremens from alcohol withdrawal, in which case benzodiazepine is indicated. Antipsychotics can be used to treat hyperactive agitation. And when it is needed to be used, we need to use them at the lowest dose and shortest duration possible. These antipsychotics are not indicated for treatment for hypoactive delirium and should not be used for these patients.
SUSAN KARTIKO: OK. Now we're going to go through the scenario for a little bit. This is a 78-year-old female with hip fracture and multiple rib fractures after MVC. On hospital day 5, she was found with altered mental status, and she is lethargic. So you did a neuro exam, and it is non-focal, and the next thing that we need to do is how to work it up.
SUSAN KARTIKO: And if you say we will obtain EKG, lab works, including ABG and CT head, then you would be correct. And the EKG shows AFib with a rate of 78. ABG is as listed, 7.36. PaCO2 of 40, PaO2 of 105, and bicarb was 24. And the CT head was done as well, showing no acute bleed or acute stroke.
SUSAN KARTIKO: When bCAM was done, it was shown that patient has positive delirium.
AMIT JOSHI: Dr. Kartiko, in that scenario, how important is the CT? I know we do it as a reflex, but I'm going to play devil's advocate. If your neurologic exam was non-focal, one might argue that it is unnecessary, but is that true?
SUSAN KARTIKO: Yes, you are correct. So you do not have to do, especially if it's non-focal, you do not have to do that. The only thing, the only caveat is-- so if the patient is comatose or altered enough, because you can still have basal ganglia stroke, which it just may or may not be focal in terms of right of left.
AMIT JOSHI: OK.
SUSAN KARTIKO: And on conversation for this patient-- again on conversation with her nurse-- the patient has not been able to sleep, it seems, well for the past two nights, due to her rib pain. And as you look at the medication, her medication includes oxy, 10 milligrams q8 prn pain; dilaudid IV 1 milligram q6 prn pain; Xanax for muscle relaxant of her rib; and amiodarone for her chronic AFib, which is her whole medication.
SUSAN KARTIKO: Looking at this medication, how would you adjust your medication to prevent her delirium? I'll give you a little bit of time to think about it, but this is what I would do. I would increase the frequency and decrease the time that it takes for her to take her pain medication. For her I would decrease her pain medication, her dose, and increase the frequency.
SUSAN KARTIKO: So I would put her on oxy 5, maybe q5 or q6 prn pain. I would give her dilaudid 0.5 milligram as opposed to 1 milligram q4, prn pain, and I would dc the Xanax altogether. I would continue her whole medication but also to take care of her rib pain, I would ask for a rib block or epidural for her rib fracture pain control. And then for sleep hygiene-- and she will need the sleep hygiene, of course-- but I can also add melatonin for sleep.
SUSAN KARTIKO: Other adjustments can include maintaining the day and night cycles, minimize the tethering, keeping her out of bed, which also makes her more awake during the day, and of course, involve family engagement. We'll pause there for this QR code to log your attendance.
AMIT JOSHI: I'll just say that first of all, this is a great review and such an important topic, and a lot of research in the last five, 10 years on this subject, and we've come so far. I mean, I think about when I trained, this is not even something that we thought we thought about. We thought if a patient were delirious, we would just flood them with medication. And that mnemonic that you described as 15 letters long, I mean there's so many adjuncts now to treat this, and recognition is clearly such an important part of it.
AMIT JOSHI: So thanks.
SUSAN KARTIKO: Yes, yes, thank you. And it is very important for patient outcome as well. All right, so the next one we will talk about acute liver failure and hepatorenal syndrome. Hepatic failure itself is divided into acute and chronic, and we'll be talking about the acute part. In acute liver failure, the duration has to be less than 26 weeks. Within that, we further divide it into hyperacute in symptoms that occur for zero to six days; acute, seven to 21 days; and subacute, 22 days to 26 weeks.
SUSAN KARTIKO: The diagnostic criteria should be for patients with INR that is 1.5 or more, patients who have abnormal LFTs, have encephalopathy, no cirrhosis or prior liver disease, and less than 26 weeks since symptom onset. Obviously the chronic part would be if they go past 26 weeks. The cause of acute liver failure-- there are many different causes. The most common one is acetaminophen overdose, and this happens in 50% of acute liver failure in the western world.
SUSAN KARTIKO: In the other part of the world, It could be from viral hepatitis. For the US, it is the acetaminophen overdose. And this is dose dependent and characterized by high amino transferase level, usually above 3,500. The next common cause of acute liver failure is idiosyncratic drug induced liver injury. This happened in 13% of acute liver injury. This is usually not dependent to the dose.
SUSAN KARTIKO: It occurs typically within six months of starting a new medication, and the most common cause of these is antibiotic, NSAID, anti-convulsion medication. The next most common is viral hepatitis. It's just 12% of the acute liver failure, and it is also caused by many different kind of viral illnesses, including hepatitis A, B, D, and E. Hepatitis C rarely causes acute liver failure.
SUSAN KARTIKO: But then there are other viruses as well, such as herpes simplex, varicella, Epstein-Barr virus, adenovirus, and CMV. The next one that can cause acute liver failure is Wilson disease, and it happens in about 5% of acute liver failure patients. Autoimmune hepatitis caused about 2% to 3%. Hypoperfusion leading to ischemia can also occur, and it happens in 1% to 2 and 1/2% of acute liver failure.
SUSAN KARTIKO: This can be caused by systemic hypotension. It could be from congestive heart failure. It could be from sepsis that has gotten out of control. It could be from venous obstruction, such as Budd-Chiari syndrome. It could be from arterial constriction from cocaine and meth overdose. And then other things that can cause acute liver failure, which is quite rare however, is acute fatty liver of pregnancy or HELLP syndrome.
SUSAN KARTIKO: Now hepatic encephalopathy, it's important to talk about within this realm because this confers to a worse prognosis and acute liver failure. And care for acute liver failure should be to prevent onset of hepatic encephalopathy or to limit its severity and reduce the risk of cerebral edema. The liver itself can hopefully get better on its own, or we can give some medication for the liver, but once the hepatic encephalopathy sets in and worsen, that's when kind of cat is out of the bag.
SUSAN KARTIKO: So hepatic encephalopathy itself is divided into different grades. The first one is grade I, and this usually the patient has mild confusion, has slurred speech, has sleep disturbances. Grade II, the patient starts to become more lethargic. They're more confused. Grade III, the patient has marked confusion, usually incoherent, however still arousable. People with grade III hepatic encephalopathy have 35% risk of developing cerebral edema.
SUSAN KARTIKO: For grade IV, patients are usually comatose, and about up to 75% of them can develop cerebral edema. The treatment for hepatic encephalopathy is to reduce cerebral edema. So we can recall back to the neurologic dysfunction and patient with TBI. The treatment is the same for the cerebral edema, such as giving hypertonic saline or giving mannitol just to delay the onset of cerebral edema.
SUSAN KARTIKO: For these patients, sometimes we want get hypothermia and maintain the temperature to 35 to 36 degrees to slow the body metabolism. And then ICP monitoring can be used in patients with evolving cerebral edema. This happened again. I'm so sorry.
AMIT JOSHI: It's OK.
SUSAN KARTIKO: Sorry.
AMIT JOSHI: In this disruptive year, we've all become used to non-cooperating computers.
SUSAN KARTIKO: I know. The treatment for acute liver failure. Patients who are critically ill should be admitted to the ICU, because they do have organ failure for this one. Patients who have acute liver failure due to acetaminophen toxicity we can administer N-acetylcysteine.
SUSAN KARTIKO: If the patient has some sort of viral infection, we can of course give them antiviral depending on what they are. Patient who has Budd-Chiari syndrome may be helped by a TIPS. However, most of acute liver failure treatment is really supportive therapy. They are very much at high risk for hypoglycemia in which case needs to be diagnosed-- worked up, diagnosed, and treated.
SUSAN KARTIKO: They are at risk for bleeding. If there is a concern for bleed, the patient needs a [? TEG ?] level, coagulation level to be checked especially if a procedure needs to be done, or a patient is actually bleeding. We certainly have to avoid hypotonic fluid resuscitation, because this can cause hyponatremia and cerebral swelling. And patient also may need ICP monitoring if there is a sign of cerebral edema, especially if their GCS really is less than 8.
SUSAN KARTIKO: Nutritional support is very important for acute liver failure patients, as this patient is in a catabolic state. Additionally, they are at high risk of developing gastric ulcer or duodenal ulcer, and so they need to be in prophylaxis for ulcer. The other treatment for acute liver failure that is unfortunately not universally available is transplantation.
SUSAN KARTIKO: Only about less than 10% of liver transplantation are performed on patients with acute liver failure. Acute liver failure affects different organ system, and the assessment and specific care that is needed is listed in this table, and we'll go through it a little bit. If the patient has acute liver failure and developed hypotension, certainly they need to be admitted in a ward that is capable to monitor the hemodynamic.
SUSAN KARTIKO: And if it needs to be in the ICU, then so be it. They usually need echocardiogram. They also need a correction if they are volume depleted. They need to have some fluid. If the problem with the hypertension is vasodilation they'll certainly need some vasopressor support. It could be that these patients also develop hypotension from low cardiac output or right ventricular failure, in which case they need amyotrophic support.
SUSAN KARTIKO: The evolving hepatic dysfunction itself can cause many different biochemical abnormalities, and we need to do a serial lab to support the patient, as well as coagulation testing. Respiratory wise, these patients are at risk of aspiration because the level of consciousnesses is altered, and so if they need to be tracheally intubated for a depressed level of consciousness, then so be it. So that needs to be done.
SUSAN KARTIKO: Patient also may develop hypoglycemia as I said before, and so serial biochemical testing is very important to maintain normoglycemia. Patient may develop hyponatremia which is then tied into having some sort of renal dysfunction. And if this is severe enough, patient may need renal replacement therapy, dialysis, or CRRT. The progressive encephalopathy is very important, and we need to do neuro checks.
SUSAN KARTIKO: And if the neuro check is not adequate, then we may need to also place intracranial monitoring for ICP measurement. And the patient definitely needs to be treated for that, again with osmotherapy, such as mannitol hyper tonic saline, temperature management, and other things that we need to do. Making sure the patient is sitting up straight, making sure they're not aspirating and causing more problem with hypoxia and hypothermia.
SUSAN KARTIKO: Patient who has acute liver failure is also at high risk for sepsis, and they may need antibiotic prophylaxis to prevent that from happening. So what is the prognosis of acute liver failure? Well, spontaneous recovery for acute liver failure is predicted by the severity of hepatic encephalopathy. Patient with grade I and grade II hepatic encephalopathy has 65% to 70% likelihood of spontaneous recovery of the liver.
SUSAN KARTIKO: However, once the patient has grade III hepatic encephalopathy, only 40% to 50% recover spontaneously. And once they have grade IV, then less than 20% of patients can have a spontaneous recovery. When dealing with patients with acute liver failure, the referral to orthotopic liver transplantation is done based on King's College Criteria. If the patient has the acute liver failure due to acetaminophen toxicity, pH is 7.3 irrespective of grade of hepatic encephalopathy meets criteria.
SUSAN KARTIKO: Or if the grade III or IV hepatic encephalopathy and has a prothrombin of more than 100 seconds and creatinine that is greater than 3.4. That's for acetaminophen toxicity. If the patient has acute liver failure due to other causes, then the criteria becomes PT, prothrombin of more than 100 second, irrespective of the hepatic encephalopathy grade. Or any of the following, which is age less than 10 or greater than 40, unfavorable disease etiology, such as non-A, non-B viral hepatitis, idiosyncratic drug reaction, Wilson's disease, and then duration of jaundice before development of encephalopathy greater than seven days.
SUSAN KARTIKO: PT greater than 50 seconds and serum bilirubin greater than 18. These are all basis for liver transplantation referral. OK. We're going to switch gear a little bit to hepatorenal syndrome. Hepatorenal syndrome is a syndrome where liver failure causes renal failure as well.
SUSAN KARTIKO: It occurs in patients with cirrhosis and portal hypertension. As the hepatic disease becomes more severe, there is progressive rise in cardiac output and fall in systemic vascular resistance. And the portal hypertension can lead to splanchnic vasodilation, which decreases the effective arterial blood volume and renal perfusion.
SUSAN KARTIKO: This renin-angiotensin system and the sympathetic nervous system are activated by the hypotension, which further reduces GFR and sodium secretion, and this then causes the renal failure. HRS developed in 18% of cirrhotic patients within one year and 39% within five years. So hepatorenal syndrome is really is more of the chronic liver failure cohort. It could happen in the acute, but it requires cirrhosis and portal hypertension, which usually fit in more into chronic liver failure.
SUSAN KARTIKO: Hepatorenal syndrome is a diagnosis of exclusion. Diagnostic criteria include increasing serum creatinine, oliguria, with the sodium that is less than 10 milli equal per liter in the urine, as well as no improvement in kidney function with crystalloid or albumin resuscitation. And the urine RBC has to be less than 50, and urine protein has to be less than 500.
SUSAN KARTIKO: And that signifies that there's no intrinsic problem with the kidney itself, and the reason the kidney is affected is because of the liver failure. There are two types of HRS. Type 1, where the creatinine doubles within two weeks and reaches at least 2.5 milligrams per deciliter, and this is more serious. And then the second one is type 2, which is the renal impairment and ascites that does not respond to diuretics.
SUSAN KARTIKO: And these are considered to be less severe renal impairment. Or in this type 2 people have a less severe renal impairment. Hepatorenal syndrome can be precipitated by a bacterial infection. And when it is clotting type 1 HRS, usually it's not better with this antibiotic therapy. The other thing that can precipitate hepatorenal syndrome is GI bleed.
SUSAN KARTIKO: If you can tell, both of these also does not help with the fact that they are both kind of causing a shock state of some sort. GIB can cause the hemorrhagic shock, and the bacterial infection can certainly go into the septic shock. The treatment for hepatorenal syndrome is to improve the liver function itself. So if it is due to alcohol, an absence of alcohol.
SUSAN KARTIKO: If it's due to viral hepatitis, we can start or continue to antiviral treatment, and as well as supportive therapy for acute liver failure if it happens in that acute liver failure cohort. And lastly, liver transplantation. Aside from those, HRS, if they are critically ill, and they are hypotensive, then we want to use pressors, such as norepi, to increase the MAP by 10 millimeter mercury and use albumin for volume expansion for at least two days in a row.
SUSAN KARTIKO: We can also add vasopressin if they are able to receive drips, meaning that they are in the ICU. If they are having hepatorenal syndrome, but their hypotension is not really meeting criteria for ICU, then we certainly can use things like midodrine, which is a pressor in the form of a pill. You can think of it that way.
SUSAN KARTIKO: Octreotide, which also can promote vasoconstriction of the splanchnic circulation, and again albumin for volume expansion. If the patient fails this medical therapy despite the pressor, despite the midodrine and they are still failing, then hemodialysis can be used as a bridge to either a liver transplantation or wait until there is recovery either on the liver side or on the kidney side.
SUSAN KARTIKO: It is also thought that TIPS sometimes work for hepatorenal syndrome. To prevent someone into developing HRS, patients have been in trials for this. So this patient can be given IV albumin for patient who have SBP, subacute bacterial peritonitis, on day 1 and day 3 of antibiotic treatment, and this has been shown to reduce renal impairment and mortality.
SUSAN KARTIKO: So a patient who comes in who comes in with subacute bacterial peritonitis, giving albumin can prevent them from developing HRS. The prognosis for HRS itself without treatment would be mortality within weeks from onset of renal impairment. This is quite severe. And the prognosis of HRS depends on the ability to reverse the liver function, or if liver transplantation is available for the patient.
SUSAN KARTIKO: That is the end of the third portion off the talk, and again, this is the QR code to log in your attendance.
AMIT JOSHI: Great. Thanks, Dr. Kartiko. I particularly appreciated the discussion of hepatorenal syndrome very-- I have always found that to be a really confusing topic, and those patients can be really frustrating, I think, in the ICU.
SUSAN KARTIKO: Right. They are very sick usually.
AMIT JOSHI: Yeah. Well, thank you so much, everyone, Dr. Kartiko especially for your SCORE School lecture, and we'll see you next week. Thanks, everyone.
SUSAN KARTIKO: Thank you.
Segment:0 .
AMIT JOSHI: Hi, everyone. It's Amit Joshi from SCORE. Welcome to SCORE School. This week, we're going to be covering organ system dysfunction, the third part of three. I'm really delighted to be introducing Dr. Susan Kartiko. She is an assistant professor of surgery at the George Washington University School of Medicine. She earned her M.D. and PhD from Texas A&M Health Science Center in Texas, then did a surgical residency at Einstein Healthcare in Philadelphia, followed by a surgical critical care fellowship at Boston University.
AMIT JOSHI: After three years at the University of Massachusetts Bay State in the division of trauma, emergency surgery, and surgical critical care, Dr. Kartiko moved to Washington, DC, where she's now at GW. Her research interests include surgical education, trauma surgery, and geriatric trauma. She's going to be covering the modules of neurologic dysfunction, pain agitation and delirium, and hepatic failure and hepatorenal syndrome.
AMIT JOSHI: Dr. Kartiko, thank you so much for joining us, and go ahead.
SUSAN KARTIKO: Thank you for having us and a warm welcome. Today we will be talking about organ dysfunction part 3, and this is the QR code to log in for your attendance. The topic that we'll be talking about today will be neurological dysfunction both trauma and non-trauma, pain delirium and agitation, and lastly, hepatic failure and hepatorenal syndrome. First, we're going to start with the neurological dysfunction.
SUSAN KARTIKO: Many surgical patient presents with neurological dysfunction, and this comes from altered mental status due to many different causes. Most common causes could be sepsis, could be from traumatic brain injury, could be from delirium, could be from spinal cord injury, et cetera. As the surgeon, we will have patients with neurological dysfunction, so we need to be able to recognize, diagnose, and intervene on neurological dysfunctions in our patients.
SUSAN KARTIKO: So first we'll discuss about neurological dysfunction in trauma patients. As usual, all patients who arrive as a trauma will need to be assessed in a systematic way. In the US and many places in the world, we use ATLS for this. ATLS dictates that all patients that come into the trauma bay needs to be assessed ABCDE-- airway with a C-spine immobilization, B for breathing, C for circulation, and then D for disability.
SUSAN KARTIKO: And this is the time that we assess our patient's neurological dysfunction, or if there is one. We usually do this by using the Glasgow Coma Scale, and all patients who have GCS less than 8 will need to have their airway protected. And then ATLS dictate that we look into the environment, such as the temperature they're in, and to expose them.
SUSAN KARTIKO: The Glasgow Coma Scale is a scale to assess a patient's level of consciousness in head trauma. Patient's GCS should be done after the patient is hemodynamically stable, or as stable as can be, and preferably not when they're on sedatives. GCS looks into three different criteria-- the eye opening, the verbal response, and motor response. Eye opening has a scale from 1 to 4, as you can see on the table.
SUSAN KARTIKO: Verbal response has a scale from 1 to 5, and motor response has a scale from 1 to 6. The lowest GCS a person can have is 3, and the highest is 15. When we determine for patient's GCS, we obtain the highest score the patient can score, also knowing that GCS can change, and it may fluctuate during a certain time. Again, with patients who have a GCS less than 8, airway protection is important, and it's to be secured.
SUSAN KARTIKO: Trauma patients who arrive with a low GCS, it could be due to many different things. So the differential diagnosis could include traumatic brain injury. However, that's not the only cause that patient may have for a neurological dysfunction in a trauma situation. End organ dysfunction, such as due to hemorrhagic shock, can also cause low GCS.
SUSAN KARTIKO: Spinal injuries should be entertained, especially if the patient is awake; however, they're not able to do the motor portion of the scale. It could also be due to drugs or medication overdose. It could be due to seizure. [? Many ?] [? aphasic ?] people have [? ICP ?] and had a seizure and that their alertness is affected. It could be that they have a seizure disorder, and that's why they're having the seizure, and when-- got into a traumatic situation, such as motor vehicle crash.
SUSAN KARTIKO: And it could be due to many different things. The neuro exam on a trauma patient would be focused on signs of trauma, especially in the head or in the spine. We should also look into pupillary exam, gross motor and sensation exam of the patient. While running the trauma, be aware of patient's vital signs, which may be showing signs of brain stem herniation, and this is called Cushing response.
SUSAN KARTIKO: Cushing response is the physiologic response to acute elevation of the intracranial pressure. The hallmark is systolic hypertension and bradycardia, and this can be accompanied by irregular respiration pattern. To prevent further elevation of the intracranial pressure, especially in the trauma bay, there are several things that can be done. If the patient is already intubated, then we can hyperventilate them through the vent.
SUSAN KARTIKO: This is only a transient response, should not be used for a prolonged effort to keep someone's ICP low. And the goal for the hyperventilation is for pCO2 between 30 and 35 millimeter mercury. It should not be any lower than that. The other thing that we can give is hyperosmolar therapy, such as hypertonic saline and mannitol. If the patient blood pressure is good enough, then we should give the patient sedation and pain control, such as opioids, and sedation can be the form of Precedex, in the form of propofol, depending on whether the patient is intubated or not.
AMIT JOSHI: Dr. Kartiko, could I ask you one question there? So a common at least multiple choice question is to prioritize those three-- hyperventilation and the hyperosmolar therapy and sedation pain control. So how would you actually put them in order of intervention?
SUSAN KARTIKO: So if the patient is intubated, the fastest way to decrease someone's ICP is via hyperventilation. But this is only to buy time for a little bit, so that we can have the hypertonic saline ready, make sure the patient has an IV, that it's secure. And then the next thing that I would use is actually hyperosmolar therapy. Sedation and pain control is also important, but sometimes these are not necessarily possible to be given if the patient has other like low blood pressure or other hemorrhagic signs.
SUSAN KARTIKO: And pain control can be given judiciously, but sedation may not be the one that we want to use, especially if the patient's GCS is already low.
AMIT JOSHI: Got it. Thank you.
SUSAN KARTIKO: When we are discussing about elevation of the intracranial pressure in trauma patients, we should understand the Monro-Kellie Doctrine The Monro-Kellie Doctrine explains the relationship of cerebrospinal fluid, blood in the brain, volume, and pressure when there is an increase in mass. This increase in mass can be in the form of tumor or blood. Intracranial pressure is unique, due to the skull preventing expansion in the event of increased intracranial mass.
SUSAN KARTIKO: When there is a new mass-- for example, blood-- the system displaces CSF and blood first, and thus there is a compensation of the volume increase to maintain a certain pressure. You can see this actually in the graph of the volume pressure curve. There is still a flat portion of the pressure graph. At a certain point, however, the system will seek to compensate, and with a small increase in mass, the pressure can increase in an exponential manner.
SUSAN KARTIKO: This is why after a certain point an increase in intracranial bleed, even by a small volume, can increase the risk of herniation very rapidly. So how do we diagnose and treat TBI? Diagnosis for traumatic brain injury-- the CT scan is the gold standard. Once TBI is diagnosed, the next thing that we do is neuro checks to determine if there is a neurological dysfunction that is worsening.
SUSAN KARTIKO: Neurosurgical intervention should be considered. However, if surgery is not indicated, prevention of secondary insult of patient's brain should be the goal. Traumatic brain injury can be categorized into two type of insults. One is the initial insult to the brain, which is the initial injury, and then the second one is a secondary insult. Patient with TBI that was for secondary insult. The secondary insult can come from extracranial sources and intracranial hypertension.
SUSAN KARTIKO: The intracranial sources can be from hypoxia, hypotension, fever. However, this whole thing as a secondary insult can worsen the outcome of TBI, much worse than the primary insult. To prevent secondary insult in TBI, we need to prevent intracranial hypertension and avoid extracranial things, such as hypotension, hypoxemia, hyperthermia or fever, and seizure.
SUSAN KARTIKO: So first we'll look into how to maintain a low ICP. The easiest thing to do, especially after a spinal cord injury is ruled out in a trauma patient, is to elevate the head of bed to 35 to 45 degree. ICP monitor can be used, especially if patient's GCS is less than 8, and neuro exam is no longer very good at that point, because the patient is comatose. Once the ICP monitor is inserted, the goal is to maintain a cerebral perfusion pressure, which is CPP.
SUSAN KARTIKO: CPP is obtained by MAP minus ICP, and we want to maintain the CPP between 60 and 70 millimeter mercury. To do this, there are two things that you can do technically. The first one is to increase the MAP, and the second one is to decrease the ICP. We typically try to decrease the ICP, especially if the MAP is already normal. If it is hypotensive, then the next thing that we need to do is maybe if it's due to hemorrhagic shock, then to give blood and to make sure that we can stop the bleed.
SUSAN KARTIKO: However, to decrease the ICP, we can do many things, and this is expanded from what we could do in the trauma bay because at this point we have imaging, and we know exactly what is wrong with the patient or presumably. So the things that we can do again is hyperosmolar therapy. We certainly can give sedation at this point, because we already know what kind of injury the patient has. Pain control becomes important as well.
SUSAN KARTIKO: If hyperosmolar therapy, sedation, and pain control is no longer able to decrease the ICP, we can venture into paralytic. However there's still-- we still need to reassess for surgical intervention. Maybe patients who didn't need to have surgery done prior, now becomes more imminent to have some sort of surgical intervention. The surgical intervention that can be done is decompressive craniotomy, which has been shown to reduce ICP and may improve outcome.
SUSAN KARTIKO: However, studies have shown that bifrontal decompressive craniotomy, while reduces ICP and ICU length of stay, has not really improved outcome. This is the MAP, the ICP part. Then the next part would be to manage the extracranial problems, including hypoxia. The goal for our patient is to prevent secondary insult is not to crank up the oxygen as high as we can but to maintain a normal paO2.
SUSAN KARTIKO: The other thing that we need to do is avoid fever, and the goal is not hypothermia but normal temperature. We also need to avoid seizure. That's why these patients are given anti-seizure prophylactically. We also need to maintain their nutritional requirement, and ASPEN guideline has said to feed the patient with TBIs within 48 hours of admission. Chlorhexidine oral care is to prevent a pneumonia.
SUSAN KARTIKO: Pneumonia of course causes hypoxia, may cause hypotension, may also cause a fever, all of which are not good for a patient with TBI. There is no role for steroids for traumatic brain injury. And the other thing that we need to do is avoid hypotonic solution to prevent cerebral edema. That means no LR, that normal saline. It's usually the one that we use for people with TBI.
SUSAN KARTIKO: The prognosis of traumatic brain injury has been studied quite extensively. There are certain things that we know, such as low initial GCS, usually confers to a worse prognosis. Increase in age is a strong independent risk factor for worse prognosis as well in TBI, and the significant increase in poor outcome for patients above 60 years old. Based on the CT scan itself, there are certain things that can determine prognostication.
SUSAN KARTIKO: We know that an abnormal CT scan in 90% of patients-- we know that there is about 90-- abnormal CT scan in 90% of patients with severe head injury. However, the absence of CT scan abnormality does not really preclude high ICP and that new lesion may develop in 40% of the patients. The other features in CT scan that confer to worse prognosis is compressed or absence of the basal cistern.
SUSAN KARTIKO: This indicates three times risk of high ICP, which of course is related to outcome. Traumatic subarachnoid hemorrhage is a worse prognosis, and it confers to two times mortality to other type of TBI. And of course midline shift confers to worse outcome as well, because that shows an increase in intracranial pressure due to MAP.
SUSAN KARTIKO: In trauma patients with concerns of spinal cord injury, the symptoms usually decrease in gross sensation or motor function in the extremities. And this can also cause tingling or decrease in sensation in their fingers or toes. Inline immobilization is very important, especially in the beginning part of the workup in the trauma bay. The spinal cord injury, the imaging that we usually get is the CT scan, usually C-spine, thoracic, and lumbar, and then MRI when there is a spinal cord injury that is suspected.
SUSAN KARTIKO: The goal of the spinal cord injury treatment is to maintain spinal cord perfusion with surgical intervention if needed. Steroid has not been shown to be beneficial in the transection injury of the spinal cord, but it could be beneficial for people who have central cord syndrome. So central cord syndrome patient in trauma, it could be that they are already narrow. They have a spinal stenosis, and the trauma causes injury, and they present as central cord syndrome patients.
SUSAN KARTIKO: Sorry, my computer just went kaput. I need to open the PowerPoint again. Sorry.
AMIT JOSHI: OK.
SUSAN KARTIKO: And then [? it ?] [? starts. ?] OK. All right now, let's discuss neurological dysfunction that is not due to trauma nor TBI. So we encounter patients with neuro-disturbances sometimes, and this can be due to many things, and we find them on the floor. And this patient usually presents with altered mental status. And this altered mental status can be due to many different things, such as end organ hypoperfusion, maybe due to hemorrhagic shock, maybe due to septic shock, maybe due to cardiogenic shock.
SUSAN KARTIKO: Other things that can cause neurological dysfunction in a surgical patient includes physiologic derangement, such as high ammonia in people who have liver failure or uremia in people who have kidney failure. Primary infection of the brain, such as meningitis and infectious encephalopathy, can also happen. Seizure can also be a cause of neurological dysfunction of surgical patients. Delirium/agitation is another cause.
SUSAN KARTIKO: And last but not least is a stroke. Patient may also have stroke, and if that's the case, then of course care needs to be done pretty quickly to render better outcome, especially for a stroke patient. For the treatment for all these patients who have altered mental status or neurologic dysfunction that are not due of trauma, the first thing that we need to do is stabilize the patient.
SUSAN KARTIKO: We can use the same mnemonic of ABC-- maintaining airway, breathing, circulation. If the mental status is bad enough, then if certain airway needs to be done, such as intubation, we should do that. And then we need to move on to diagnosing by going through the workup, looking at labs, looking at chest X-ray, looking at EKG, CT head if it's needed. And of course, we need treat the underlying cause.
SUSAN KARTIKO: So that's the end of the neurological dysfunction part of the module. This is again the QR code to login in--
AMIT JOSHI: [INAUDIBLE]. Thank you. I'll just re-emphasize the point you made, which is how important the intensivist or the surgeon managing the global status of the patient can be in treating neurologic dysfunction. So it's something I know that our critical care faculty always emphasize in the unit, but this is why critical care is such an important part of surgery.
AMIT JOSHI: The neurosurgeons may be managing the brain or the spine. The orthopedists might be managing the extremity injuries, but we are still responsible for maintaining the organism as a whole. And so that was a nice review of avoidance of secondary injury in particular. Thank you.
SUSAN KARTIKO: Thank you, and I couldn't agree more with the sentiment. OK, so the next topic we'll be talking about is pain, agitation, and delirium. The first thing I'll be talking about is pathophysiology of surgical pain. Pain is due to nocioceptive activation via the prostaglandins, interleukins, cytokines, and neurotrophins. In injury, the decrease in tissue pH, oxygen tension, increase in lactic acid, along with an increase in peripheral granulocytes can cause pain at rest and increased response to stimuli at the site of injury.
SUSAN KARTIKO: And this is the primary hyperalgesia. Central sensitization can in turn amplify the noxious input during and after the surgery. To assess for pain, we should ask our patients the location of the pain. Patient comes in with a certain pain, pain in the belly, pain in the leg, and we should assess them. What is the location of the pain, the duration of the pain, the quality of the pain, and what makes it better or worse, and then the intensity of the pain.
SUSAN KARTIKO: Quality of pain can be divided into somatic, visceral, and neuropathic pain. Somatic pains are usually dull and aching. They are usually well localized, and these are the pains that are caused by bone fracture, bone mets, muscle strain. So there is a localized area where [? they're ?] [? saying, ?] the area that may be injured. Visceral pain-- it could be dull or sharp.
SUSAN KARTIKO: It could be collicky, comes and goes. It could be well localized or it could be referred. And these are more of the gastritis pain, gallstone pain, pancreatitis pain. Then there is neuropathic pain. This is more a burning sensation, lancinating, itching sensation. And it usually follows the path of the nerve, and this can be from herpes zoster type of pain, spinal disk pain, diabetes pain, such as diabetic neuropathy.
SUSAN KARTIKO: The intensity of pain is usually communicated in a scale. The most common scale is American scale from 0 to 10. Usually we say what is the worst pain that you can have, and that would be 10. And be careful with that, because people may not have had pain. And so we usually say things like, if you can imagine yourself being hit by a truck, that would be number 10.
SUSAN KARTIKO: Or if you've given birth before vaginally, that would be number 10. And then we also ask during our interview what kind of treatment the patient has tried. Oh, I take Tylenol, doc. Or I take ibuprofen or I put warm compresses. Does that work at all? The last thing, and usually we kind of skip it in our patient, is that the impact of pain on life, whether the pain is affecting the activity of daily living.
SUSAN KARTIKO: Does it affect your sleep? Does it wake you up from sleep? Does it affect your eating? Does the pain make you not want to eat at all? Does it affect how you move? Do you move in a certain way now because your hip is bothering you, or your back is bothering you. And then lastly, that it's more important to our patient is whether the pain affects their daily working life.
SUSAN KARTIKO: The management of pain, especially for surgical pain, should start during the pre-op time. This includes setting expectations for the pain after the surgery. Pain management should not be an afterthought. Additionally, pain management should depend on the type of surgery that is being performed and the setting i.e. emergency surgery or urgent surgery may have more pain associated with it compared to elective.
SUSAN KARTIKO: The type of surgery being performed, if it's a laparoscopic type of surgery versus open surgery. The expectation of pain should be given prior to the actual surgery. To control pain, it is recommended that we use multimodal pain control, meaning utilizing medication that target different receptors and using different modalities, such as blocks to minimize the use of opioids.
SUSAN KARTIKO: Of course, nowadays we have the opioid epidemic, and all efforts should be done to decrease that, and that we use many different things to control pain. The different kinds of medication that can be used to alleviate pain include Tylenol or acetaminophen; NSAIDs, such as ibuprofen and Celebrex. We can use muscle relaxant antineuropathic pain medications as gabapentin, and of course opioid.
SUSAN KARTIKO: Pain should be viewed as a continuous thing with peaks and valleys, so pain needs to be assessed routinely, and pain medication administration needs to be adjusted depending on the pain that the patient is having. Just because it's usual for a surgical patient to have oxy 5 every 5 to 6 hours, that does not mean that works for everybody. It also does not mean that that alone should be able to treat all the peaks and valleys, so we have to arrange our pain medication administration based on the pain that the patient is feeling at the time.
SUSAN KARTIKO: Pain is very important to be controlled appropriately to avoid delirium and agitation and allow for appropriate recovery from surgery or injury. This is a table of different pain control modalities. If you look at the first column, there is a different technique, and the first technique is neuroaxial opioid analgesia. This is more into the epidural and spinal anesthesia routes, and we can administer opioids through it along with local anesthetic.
SUSAN KARTIKO: So the common medication we use in there would be the fentanyl in the epidural or maybe even dilaudid or morphine. And this has been shown to improve pain relief compared to pre-incisional, oral, or IV or intramuscular administration, so it is quite good to use for a certain type of operation. The next one that we can use is peripheral or central regional analgesia or blocks.
SUSAN KARTIKO: We're talking about intercostal blocks for rib fracture, plexus blocks, local anesthetic infiltration or in the incision, when we're making incision. And the common medication we use is bupivicaine, ropivicaine. It could also be lidocaine if it's for the local anesthetic. And the purpose of this is to reduce inflammation, alleviate pain, and reduce analgesic requirement later on including opioid. It has been shown to reduce length of stay, especially for rib fracture, and improve recovery time.
SUSAN KARTIKO: Next medication is non-opioid analgesic. We talked about it briefly before. Acetaminophen, NSAID, antidepressant, alpha-2 agonist, anticonvulsant such as gabapentin, and NMDA receptor, which is ketamine that can be given as IV medication either drip or as boluses. And lidocaine, which can also be given as drip or boluses. And this is all done to reduce the opioid requirement.
SUSAN KARTIKO: The next one is the parenteral analgesic, which is the IV opioid. And we have morphine, fentanyl, dilaudid, sufentanil. It is important to use the lowest dose possible for this, as well for the oral opioid analgesic, which includes oxycodone, tramadol, hydrocodone, morphine, and dilaudid. And these can also be paired with acetaminophen in the form of Percocet and Vicodin.
SUSAN KARTIKO: All right, so that would be the portion for the pain. Next we're going to talk about agitation and delirium. Delirium itself is a disturbance of consciousness. It is marked with inattention, accompanied by a change in cognition or perceptual disturbance. So they can have some hallucination that develop over a short period of time. So hours, days, and fluctuates over time.
SUSAN KARTIKO: The etiology of this multifactorial there are thoughts that some people who already have anatomic deficits are more prone to it. And then the other thing that could be the cause of delirium is neurotransmitter abnormalities. And this could be in the form of derangement in level of serotonin, acetylcholine, dopamine, or other neurotransmitter. And this can be due to systemic disease, toxic agents, withdrawal, such as withdrawal from alcohol, withdrawal from benzo, hypoxia, metabolic disturbances, psychoactive, and pain medication.
SUSAN KARTIKO: The outcome of delirium is the one that makes it a very important part for us to understand. Patients who have delirium have increased ventilator days, ICU days, and hospital length of stay, which all translates to increased costs for the patients and also for the health care in general. It is also associated with higher mortality both in hospital and after discharge. Patients who develop delirium also have a greater long term cognitive dysfunction, which is devastating for the patient.
SUSAN KARTIKO: To prevent delirium, we need to recognize the risk factor and focus our effort in modifying these risk factors, because the best way to treat delirium is prevention. So once we know the risk factor, we can modify these and hopefully prevent delirium from setting in at all. So the risk factor can be-- the mnemonic is I CAN STOP A DELIRIUM.
SUSAN KARTIKO: But as we go through this, it will make sense more than trying to memorize from a mnemonic. So the first one is impairment in ADL function, sleep and hearing or vision or sensory. This is basically everybody who is admitted to the hospital, because we always prevent them from getting out of bed, maybe, because we don't want them to fall. We certainly don't want them take a shower on their own. They have to always call the nurse.
SUSAN KARTIKO: Sometimes they couldn't even go to the bathroom on their own. Their sleep is disturbed because they're not in their own bed or in their own house. Sometimes a hearing aid is not working, or it needs more battery that nobody can change for them. And sometimes their glasses are lost, and all these can increase the risk of delirium. The other thing that makes it a risk factor is the patient already has some CNS pathology, such as stroke prior, such as having dementia or depression.
SUSAN KARTIKO: Or if they have multiple comorbidities, such as hypertension, diabetes, hyperlipidemia, anxiety, depression. All that combined can increase their risk of delirium. Alcohol and drug withdrawal is a big risk factor for delirium. Older age is also a risk factor, especially over 70 years old. New tethers, such as restraints, Foley catheter, IV fluid, NG tube, telemetry cables, can increase risk for delirium.
SUSAN KARTIKO: Surgery is an independent risk factor for deliriums, as well as trauma. Toxins is another one. Opioid use is a risk factor for delirium. However, uncontrolled pain is also a risk factor for delirium. Polypharmacies, especially for patients who are on benzodiazepine, anticholinergics, antihistamine, antipsychotic.
SUSAN KARTIKO: Anesthesia in general can increase delirium, risk for delirium. Deficiency in vitamins, especially B12, folate, and niacin. Exposure to drugs, especially psychotropic drugs. Hyper or hypothyroidism. Environmental changes. Low PO2 states, such as people who had a heart attack, or people who had PE, hypoxia from pneumonia, or having anemia.
SUSAN KARTIKO: Acute or chronic infection can cause delirium. Retention of urine or feces can cause delirium. ICU admission and institutional residences can increase delirium. Undernutrition or dehydration can increase the risk of delirium. And lastly, metabolic derangement of any kind. So there's quite a bit of risk factor, but these are all modifiable if we go through them one by one.
SUSAN KARTIKO: There are three types of delirium. Hyperactive, which is the one that we are very familiar with. A patient usually is restless and agitated, and/or agitated. And then there's hypoactive delirium, where patients are lethargic and apathetic. This is actually more associated with a higher mortality, because usually they are underdiagnosed. And then the third type is mixed delirium, where the patient has periods of both hyperactivity and hypoactivity.
SUSAN KARTIKO: To diagnose delirium, we can do a screening on our patient using CAM-ICU or bCAM for patients with a [? 4. ?] Both CAM-ICU and bCAM are pretty similar in that it is divided into four parts. And first we need to assess if the confusion is acute, unless it's on or off. If the patient has a stable baseline confusion all the time, he or she may have dementia and not really actually delirium.
SUSAN KARTIKO: So if it's yes, then we go to the second question. The second question measures for inattention. The test asks for the patient to squeeze or touch their hands when the toucher says the letter A in the sequence of letter, as you can see there, SAVEAHAART or CASABLANCA, and see how many times that there is error in that. If there's only zero to two errors, then the patient does not have delirium. However if there are more than two errors, then we move on to the next stage.
SUSAN KARTIKO: This part we want to measure-- we want to check the level of consciousness. If the patient-- and we do that using the RASS score. If the RASS score is other than zero, we can stop the test, and we can say that the delirium is present. If the RASS is zero, then we move on to disorganized thinking check and ask the questions, such as will a stone float on water? Are there fish in the sea?
SUSAN KARTIKO: Does one pound weigh more than two? Can you use a hammer to pound a nail? And if the patient has errors, there are more than one, then we can say that the patient has delirium. As I said, prior treatment for delirium, that prevention is best. And for this to happen, we need to have an interdisciplinary approach from the nursing staff, the nursing aide, geriatrician, the surgical team, the phlebotomist, the pharmacist, and most importantly, it's the family.
SUSAN KARTIKO: Nowadays it's difficult with COVID-19, but before that and hopefully after COVID-19, we try to incorporate family into taking care of the patient, and this helps tremendously to establish normalcy in their lives, so that they do not develop delirium. We also need to recognize and treat the precipitating factors and avoid medication that can worsen delirium. And this we can do by maintaining day and day/night cycles, opening their windows, turning on the TV or noise or radio during the day, and turning off TV and turning off the radio at night so they can sleep.
SUSAN KARTIKO: We want to minimize tethers. You want to avoid infection, meaning Foley. We can take out Foley as soon as that is indicated and not one day more. Pharmacological management of delirium is not really supported by strong evidence. In particular, benzodiazepines should not be used to treat agitation at all, because they can increase delirium.
SUSAN KARTIKO: The only exception to this is when the patient has delirium tremens from alcohol withdrawal, in which case benzodiazepine is indicated. Antipsychotics can be used to treat hyperactive agitation. And when it is needed to be used, we need to use them at the lowest dose and shortest duration possible. These antipsychotics are not indicated for treatment for hypoactive delirium and should not be used for these patients.
SUSAN KARTIKO: OK. Now we're going to go through the scenario for a little bit. This is a 78-year-old female with hip fracture and multiple rib fractures after MVC. On hospital day 5, she was found with altered mental status, and she is lethargic. So you did a neuro exam, and it is non-focal, and the next thing that we need to do is how to work it up.
SUSAN KARTIKO: And if you say we will obtain EKG, lab works, including ABG and CT head, then you would be correct. And the EKG shows AFib with a rate of 78. ABG is as listed, 7.36. PaCO2 of 40, PaO2 of 105, and bicarb was 24. And the CT head was done as well, showing no acute bleed or acute stroke.
SUSAN KARTIKO: When bCAM was done, it was shown that patient has positive delirium.
AMIT JOSHI: Dr. Kartiko, in that scenario, how important is the CT? I know we do it as a reflex, but I'm going to play devil's advocate. If your neurologic exam was non-focal, one might argue that it is unnecessary, but is that true?
SUSAN KARTIKO: Yes, you are correct. So you do not have to do, especially if it's non-focal, you do not have to do that. The only thing, the only caveat is-- so if the patient is comatose or altered enough, because you can still have basal ganglia stroke, which it just may or may not be focal in terms of right of left.
AMIT JOSHI: OK.
SUSAN KARTIKO: And on conversation for this patient-- again on conversation with her nurse-- the patient has not been able to sleep, it seems, well for the past two nights, due to her rib pain. And as you look at the medication, her medication includes oxy, 10 milligrams q8 prn pain; dilaudid IV 1 milligram q6 prn pain; Xanax for muscle relaxant of her rib; and amiodarone for her chronic AFib, which is her whole medication.
SUSAN KARTIKO: Looking at this medication, how would you adjust your medication to prevent her delirium? I'll give you a little bit of time to think about it, but this is what I would do. I would increase the frequency and decrease the time that it takes for her to take her pain medication. For her I would decrease her pain medication, her dose, and increase the frequency.
SUSAN KARTIKO: So I would put her on oxy 5, maybe q5 or q6 prn pain. I would give her dilaudid 0.5 milligram as opposed to 1 milligram q4, prn pain, and I would dc the Xanax altogether. I would continue her whole medication but also to take care of her rib pain, I would ask for a rib block or epidural for her rib fracture pain control. And then for sleep hygiene-- and she will need the sleep hygiene, of course-- but I can also add melatonin for sleep.
SUSAN KARTIKO: Other adjustments can include maintaining the day and night cycles, minimize the tethering, keeping her out of bed, which also makes her more awake during the day, and of course, involve family engagement. We'll pause there for this QR code to log your attendance.
AMIT JOSHI: I'll just say that first of all, this is a great review and such an important topic, and a lot of research in the last five, 10 years on this subject, and we've come so far. I mean, I think about when I trained, this is not even something that we thought we thought about. We thought if a patient were delirious, we would just flood them with medication. And that mnemonic that you described as 15 letters long, I mean there's so many adjuncts now to treat this, and recognition is clearly such an important part of it.
AMIT JOSHI: So thanks.
SUSAN KARTIKO: Yes, yes, thank you. And it is very important for patient outcome as well. All right, so the next one we will talk about acute liver failure and hepatorenal syndrome. Hepatic failure itself is divided into acute and chronic, and we'll be talking about the acute part. In acute liver failure, the duration has to be less than 26 weeks. Within that, we further divide it into hyperacute in symptoms that occur for zero to six days; acute, seven to 21 days; and subacute, 22 days to 26 weeks.
SUSAN KARTIKO: The diagnostic criteria should be for patients with INR that is 1.5 or more, patients who have abnormal LFTs, have encephalopathy, no cirrhosis or prior liver disease, and less than 26 weeks since symptom onset. Obviously the chronic part would be if they go past 26 weeks. The cause of acute liver failure-- there are many different causes. The most common one is acetaminophen overdose, and this happens in 50% of acute liver failure in the western world.
SUSAN KARTIKO: In the other part of the world, It could be from viral hepatitis. For the US, it is the acetaminophen overdose. And this is dose dependent and characterized by high amino transferase level, usually above 3,500. The next common cause of acute liver failure is idiosyncratic drug induced liver injury. This happened in 13% of acute liver injury. This is usually not dependent to the dose.
SUSAN KARTIKO: It occurs typically within six months of starting a new medication, and the most common cause of these is antibiotic, NSAID, anti-convulsion medication. The next most common is viral hepatitis. It's just 12% of the acute liver failure, and it is also caused by many different kind of viral illnesses, including hepatitis A, B, D, and E. Hepatitis C rarely causes acute liver failure.
SUSAN KARTIKO: But then there are other viruses as well, such as herpes simplex, varicella, Epstein-Barr virus, adenovirus, and CMV. The next one that can cause acute liver failure is Wilson disease, and it happens in about 5% of acute liver failure patients. Autoimmune hepatitis caused about 2% to 3%. Hypoperfusion leading to ischemia can also occur, and it happens in 1% to 2 and 1/2% of acute liver failure.
SUSAN KARTIKO: This can be caused by systemic hypotension. It could be from congestive heart failure. It could be from sepsis that has gotten out of control. It could be from venous obstruction, such as Budd-Chiari syndrome. It could be from arterial constriction from cocaine and meth overdose. And then other things that can cause acute liver failure, which is quite rare however, is acute fatty liver of pregnancy or HELLP syndrome.
SUSAN KARTIKO: Now hepatic encephalopathy, it's important to talk about within this realm because this confers to a worse prognosis and acute liver failure. And care for acute liver failure should be to prevent onset of hepatic encephalopathy or to limit its severity and reduce the risk of cerebral edema. The liver itself can hopefully get better on its own, or we can give some medication for the liver, but once the hepatic encephalopathy sets in and worsen, that's when kind of cat is out of the bag.
SUSAN KARTIKO: So hepatic encephalopathy itself is divided into different grades. The first one is grade I, and this usually the patient has mild confusion, has slurred speech, has sleep disturbances. Grade II, the patient starts to become more lethargic. They're more confused. Grade III, the patient has marked confusion, usually incoherent, however still arousable. People with grade III hepatic encephalopathy have 35% risk of developing cerebral edema.
SUSAN KARTIKO: For grade IV, patients are usually comatose, and about up to 75% of them can develop cerebral edema. The treatment for hepatic encephalopathy is to reduce cerebral edema. So we can recall back to the neurologic dysfunction and patient with TBI. The treatment is the same for the cerebral edema, such as giving hypertonic saline or giving mannitol just to delay the onset of cerebral edema.
SUSAN KARTIKO: For these patients, sometimes we want get hypothermia and maintain the temperature to 35 to 36 degrees to slow the body metabolism. And then ICP monitoring can be used in patients with evolving cerebral edema. This happened again. I'm so sorry.
AMIT JOSHI: It's OK.
SUSAN KARTIKO: Sorry.
AMIT JOSHI: In this disruptive year, we've all become used to non-cooperating computers.
SUSAN KARTIKO: I know. The treatment for acute liver failure. Patients who are critically ill should be admitted to the ICU, because they do have organ failure for this one. Patients who have acute liver failure due to acetaminophen toxicity we can administer N-acetylcysteine.
SUSAN KARTIKO: If the patient has some sort of viral infection, we can of course give them antiviral depending on what they are. Patient who has Budd-Chiari syndrome may be helped by a TIPS. However, most of acute liver failure treatment is really supportive therapy. They are very much at high risk for hypoglycemia in which case needs to be diagnosed-- worked up, diagnosed, and treated.
SUSAN KARTIKO: They are at risk for bleeding. If there is a concern for bleed, the patient needs a [? TEG ?] level, coagulation level to be checked especially if a procedure needs to be done, or a patient is actually bleeding. We certainly have to avoid hypotonic fluid resuscitation, because this can cause hyponatremia and cerebral swelling. And patient also may need ICP monitoring if there is a sign of cerebral edema, especially if their GCS really is less than 8.
SUSAN KARTIKO: Nutritional support is very important for acute liver failure patients, as this patient is in a catabolic state. Additionally, they are at high risk of developing gastric ulcer or duodenal ulcer, and so they need to be in prophylaxis for ulcer. The other treatment for acute liver failure that is unfortunately not universally available is transplantation.
SUSAN KARTIKO: Only about less than 10% of liver transplantation are performed on patients with acute liver failure. Acute liver failure affects different organ system, and the assessment and specific care that is needed is listed in this table, and we'll go through it a little bit. If the patient has acute liver failure and developed hypotension, certainly they need to be admitted in a ward that is capable to monitor the hemodynamic.
SUSAN KARTIKO: And if it needs to be in the ICU, then so be it. They usually need echocardiogram. They also need a correction if they are volume depleted. They need to have some fluid. If the problem with the hypertension is vasodilation they'll certainly need some vasopressor support. It could be that these patients also develop hypotension from low cardiac output or right ventricular failure, in which case they need amyotrophic support.
SUSAN KARTIKO: The evolving hepatic dysfunction itself can cause many different biochemical abnormalities, and we need to do a serial lab to support the patient, as well as coagulation testing. Respiratory wise, these patients are at risk of aspiration because the level of consciousnesses is altered, and so if they need to be tracheally intubated for a depressed level of consciousness, then so be it. So that needs to be done.
SUSAN KARTIKO: Patient also may develop hypoglycemia as I said before, and so serial biochemical testing is very important to maintain normoglycemia. Patient may develop hyponatremia which is then tied into having some sort of renal dysfunction. And if this is severe enough, patient may need renal replacement therapy, dialysis, or CRRT. The progressive encephalopathy is very important, and we need to do neuro checks.
SUSAN KARTIKO: And if the neuro check is not adequate, then we may need to also place intracranial monitoring for ICP measurement. And the patient definitely needs to be treated for that, again with osmotherapy, such as mannitol hyper tonic saline, temperature management, and other things that we need to do. Making sure the patient is sitting up straight, making sure they're not aspirating and causing more problem with hypoxia and hypothermia.
SUSAN KARTIKO: Patient who has acute liver failure is also at high risk for sepsis, and they may need antibiotic prophylaxis to prevent that from happening. So what is the prognosis of acute liver failure? Well, spontaneous recovery for acute liver failure is predicted by the severity of hepatic encephalopathy. Patient with grade I and grade II hepatic encephalopathy has 65% to 70% likelihood of spontaneous recovery of the liver.
SUSAN KARTIKO: However, once the patient has grade III hepatic encephalopathy, only 40% to 50% recover spontaneously. And once they have grade IV, then less than 20% of patients can have a spontaneous recovery. When dealing with patients with acute liver failure, the referral to orthotopic liver transplantation is done based on King's College Criteria. If the patient has the acute liver failure due to acetaminophen toxicity, pH is 7.3 irrespective of grade of hepatic encephalopathy meets criteria.
SUSAN KARTIKO: Or if the grade III or IV hepatic encephalopathy and has a prothrombin of more than 100 seconds and creatinine that is greater than 3.4. That's for acetaminophen toxicity. If the patient has acute liver failure due to other causes, then the criteria becomes PT, prothrombin of more than 100 second, irrespective of the hepatic encephalopathy grade. Or any of the following, which is age less than 10 or greater than 40, unfavorable disease etiology, such as non-A, non-B viral hepatitis, idiosyncratic drug reaction, Wilson's disease, and then duration of jaundice before development of encephalopathy greater than seven days.
SUSAN KARTIKO: PT greater than 50 seconds and serum bilirubin greater than 18. These are all basis for liver transplantation referral. OK. We're going to switch gear a little bit to hepatorenal syndrome. Hepatorenal syndrome is a syndrome where liver failure causes renal failure as well.
SUSAN KARTIKO: It occurs in patients with cirrhosis and portal hypertension. As the hepatic disease becomes more severe, there is progressive rise in cardiac output and fall in systemic vascular resistance. And the portal hypertension can lead to splanchnic vasodilation, which decreases the effective arterial blood volume and renal perfusion.
SUSAN KARTIKO: This renin-angiotensin system and the sympathetic nervous system are activated by the hypotension, which further reduces GFR and sodium secretion, and this then causes the renal failure. HRS developed in 18% of cirrhotic patients within one year and 39% within five years. So hepatorenal syndrome is really is more of the chronic liver failure cohort. It could happen in the acute, but it requires cirrhosis and portal hypertension, which usually fit in more into chronic liver failure.
SUSAN KARTIKO: Hepatorenal syndrome is a diagnosis of exclusion. Diagnostic criteria include increasing serum creatinine, oliguria, with the sodium that is less than 10 milli equal per liter in the urine, as well as no improvement in kidney function with crystalloid or albumin resuscitation. And the urine RBC has to be less than 50, and urine protein has to be less than 500.
SUSAN KARTIKO: And that signifies that there's no intrinsic problem with the kidney itself, and the reason the kidney is affected is because of the liver failure. There are two types of HRS. Type 1, where the creatinine doubles within two weeks and reaches at least 2.5 milligrams per deciliter, and this is more serious. And then the second one is type 2, which is the renal impairment and ascites that does not respond to diuretics.
SUSAN KARTIKO: And these are considered to be less severe renal impairment. Or in this type 2 people have a less severe renal impairment. Hepatorenal syndrome can be precipitated by a bacterial infection. And when it is clotting type 1 HRS, usually it's not better with this antibiotic therapy. The other thing that can precipitate hepatorenal syndrome is GI bleed.
SUSAN KARTIKO: If you can tell, both of these also does not help with the fact that they are both kind of causing a shock state of some sort. GIB can cause the hemorrhagic shock, and the bacterial infection can certainly go into the septic shock. The treatment for hepatorenal syndrome is to improve the liver function itself. So if it is due to alcohol, an absence of alcohol.
SUSAN KARTIKO: If it's due to viral hepatitis, we can start or continue to antiviral treatment, and as well as supportive therapy for acute liver failure if it happens in that acute liver failure cohort. And lastly, liver transplantation. Aside from those, HRS, if they are critically ill, and they are hypotensive, then we want to use pressors, such as norepi, to increase the MAP by 10 millimeter mercury and use albumin for volume expansion for at least two days in a row.
SUSAN KARTIKO: We can also add vasopressin if they are able to receive drips, meaning that they are in the ICU. If they are having hepatorenal syndrome, but their hypotension is not really meeting criteria for ICU, then we certainly can use things like midodrine, which is a pressor in the form of a pill. You can think of it that way.
SUSAN KARTIKO: Octreotide, which also can promote vasoconstriction of the splanchnic circulation, and again albumin for volume expansion. If the patient fails this medical therapy despite the pressor, despite the midodrine and they are still failing, then hemodialysis can be used as a bridge to either a liver transplantation or wait until there is recovery either on the liver side or on the kidney side.
SUSAN KARTIKO: It is also thought that TIPS sometimes work for hepatorenal syndrome. To prevent someone into developing HRS, patients have been in trials for this. So this patient can be given IV albumin for patient who have SBP, subacute bacterial peritonitis, on day 1 and day 3 of antibiotic treatment, and this has been shown to reduce renal impairment and mortality.
SUSAN KARTIKO: So a patient who comes in who comes in with subacute bacterial peritonitis, giving albumin can prevent them from developing HRS. The prognosis for HRS itself without treatment would be mortality within weeks from onset of renal impairment. This is quite severe. And the prognosis of HRS depends on the ability to reverse the liver function, or if liver transplantation is available for the patient.
SUSAN KARTIKO: That is the end of the third portion off the talk, and again, this is the QR code to log in your attendance.
AMIT JOSHI: Great. Thanks, Dr. Kartiko. I particularly appreciated the discussion of hepatorenal syndrome very-- I have always found that to be a really confusing topic, and those patients can be really frustrating, I think, in the ICU.
SUSAN KARTIKO: Right. They are very sick usually.
AMIT JOSHI: Yeah. Well, thank you so much, everyone, Dr. Kartiko especially for your SCORE School lecture, and we'll see you next week. Thanks, everyone.
SUSAN KARTIKO: Thank you.
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The cadmore media player is a professional video and audio player experience designed to deliver media as well as relevant transcript, segmentation, and metadata. On the screen is a traditional html video player with buttons such as play, pause, forward, captioning, language and play speed selection and more. Adjacent to the video player are generally tabs, one of which shows a scrolling transcript of the video and the other shows any segmentation of the media, sometimes referred to as chapters. At the top of the video is a menu bar containing an Explore button and Tools button. The Explore button allows you to dig deeper into the video by opening up an explore dialog which contains tabs for a visual navigation of the video using thumbnails, an about tab which contains rich metadata about the media, a segments tab which contains further information about the video, and a related tab which contains links to other media related to this media. The tools button opens a menu with options for sharing the media on social media, creating bookmarking links, creating embed codes for your website, generating citations, and more.
Keyboard Shortcuts
Keyboard shortcuts only work while you are in forms mode. By entering forms mode, you will be able to quickly access portions of the media player with single key commands.
Spacebar: Play/Pause Toggle
I: Info Menu,
O: Tools Menu
T: Transcript Tab,
S: Segments Tab
F: Forward 15,
R: Rewind 15
L: Languages,
P: Playspeed
M: Mute Toggle,
V: Volume Bar
N: Video Only Toggle,
B: Full Screen Toggle
C: Captions Toggle
Escape: Closes dialogs and menus / Exits Player
Z: Next Transcript Chapter
X: Previous Transcript Chapter
Q: Next Transcript Paragraph
W: Previous Transcript Paragraph
Entire Media
Segment(s)
Custom Clip
Start At:
End At:
Embed Size
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You Size - Responsive
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We Size - Responsive
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Picture Overlay Popup
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400 x 225
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512 x 288
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400 x 700
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768 x 1024
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1024 x 512
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1280 x 608
Form Title Cite
No citation provided.
Info
Segments
Related
Thumbnails
Exit Clip Mode
You have requested to see a portion of the video outside of the clip.
Click OK to switch to the full video or click if you would like to stay inside the clip. You can always go back to the clip with Tools and Clip Mode