Case Reports in Anesthesia

Blog with interesting cases and/or problems related to anesthesia with discussion based on best evidence in the literature.

May 10, 2017

35 year old female with history of alcohol abuse

The other day a 35 year old female presented for surgery for lipoma excision from the posterior neck.  She reported a history of severe alcohol abuse in the past for which she was taking naltrexone 100mg qd.  The patient also reported a severe allergy to all steroids.  When I asked for details, she reported that she had severe manic exacerbations with steroids and that this had happened with a one time dose given prior to surgery in the past.  The patient had also experienced at least two seizures in the past, one occurring after surgery.  She was told that this seizure could have been related to the anesthetic she had.  She also reported another seizure episode in the past related to severe depletion of vitamin B12.  She was taking several medications for anxiety, bipolar, alcoholism and PTSD.  These included:

  • Seroquel
  • Tegretol
  • Prozac
  • Prazosin
  • Klonipin
In addition, the patient that she was concerned because in the past, she had experienced very unpleasant emergence anxiety and agitation which she hoped to avoid.


There were several issues that played a role in choosing an anesthetic for this patient. First she requested that she did not receive a steroid which I commonly give to female patients (especially non smokers) as they are at increased risk for PONV.  In addition, She was medicated with naltrexone for alcoholism.  Therefore, there was likely to be challenges with pain control in this patient.  Lastly, the patient had had previous seizures following anesthesia during emergence as reported.  She was on a number of medications that could potentially also activate her liver enzymes causing her to be a rapid metabolizer of anesthetics such as propofol, midazolam and fentanyl.

This patient described a past experience of severe agitation and anxiety upon emergence.  Emergence delirium (ED) is not uncommon in pediatrics. However, it has not been well studied in adults.  One review of the literature  estimated an incidence of 3% in adult patients. Another study found an incidence of 4.7% among adult patients [1].  However, in those at risk for PTSD an incidence of 20% is more likely [3].  Emergence delirium in adults can be a significant problem as they are capable of self injury.  A recent case report details a severe episode of emergence delirium in a patient with PTSD [4], and subsequent case where changes were made to help mitigate this issue.  In this patient with a self described episode of emergence delirium and history of PTSD and bipolar disorder, several considerations would be important.  One consideration is the recommendation to avoid midazolam in particular in this patient group.  Some literature suggests that Midazolam in particular can enhance the memory of events surrounding the trauma [5].  If a benzodiazepine is desired, lorazepam may be preferred.  While it has been traditional teaching that ketamine can excerbate PTSD, and should be avoided during anesthesia in these patients, recent literature suggests that ketamine may not be a problem [6], or may be helpful in the prevention of PTSD [7].  Currently, prazosin, an alpha 1 blocker is used in the treatment for PTSD, but also is effective in the treatment in reducing alcohol intake in alcoholics.  Therefore, it would be important to verify that this patient continued to take this medication on their usual schedule prior to anesthesia. Prazosin, as an alpha 1 blocker, can cause sudden drops in blood pressure, and this is particularly problematic when patients stand up suddenly.  In pediatrics, there is quite a large amount of literature looking at interventions that can prevent or decrease the chances of ED. Propofol decreased the incidence from 38% after sevoflurane to 0% in pediatrics.  In the pediatric literature, other studies have corroborated the benefit of propofol in reducing ED. In adults, propofol also was able to decrease the incidence of ED, from 45% to 10% [10]. Another study in the pediatric literature showed that 2 mck/kg of IV Clonidine after induction significantly reduced the incidence of ED. Like Clonidine, Dexmedetomidine may also be a useful (although expensive) adjuvant to help prevent ED.  Given that the patient had already experienced a significantly negative ED event in the past, had a post anesthetic seizure, and was also allergic to steroids, so that decadron was unavailable for PONV prophylaxis, I opted to utilize a propofol infusion for anesthesia maintenance.  Unfortunately, in a patient taking naltrexone for alcoholism, maintaining anesthesia with routine anesthetic dosages could be fraught with problems.  Therefore, I opted to utilize a BIS monitor as an aid in verifying the depth of anesthesia. The BIS system is a proprietary system using data from a processed EEG signal to produce a dimentionless number that correlates with the depth of anesthesia in a sense. It is presumed that a number between 40 and 60 represents general anesthesia and would thus have a low incidence of recall.  It is not clear if an alcoholic or patient who is taking naltrexone will respond in the same fashion to a typical anesthetic.  In this patient, 200 mg of propofol was given for induction along with 100 mcg of fentanyl and 2 mg of versed.  The BIS went from 87 to 34.  This change in BIS was as expected.  Shortly thereafter, with an infusion of propofol running at 200 mcg/kg/min and the BIS reading 34, an injection of local anesthetic by the surgeon was performed at the site of the lipoma.  The patient immediately started moving requiring an additional bolus of propofol and another 100 mcg of fentanyl.  This would be an atypical response at a BIS of 34.  However, given that propofol does not inhibit spinal reflexes as well as (if at all) the potent inhalation agents, this could be considered within normal limits.  Given the patient movement at a BIS of 34, the BIS was maintained in the high 30's for the remainder of the very short case.  A propofol infusion of 200 mcg/kg/min was sufficient.  after 30 min the case was over and the BIS reading was 36.  The propofol infusion was discontinued and in 4 minutes, the BIS had jumped from 36 to 74 and the patient began responding to commands and was extubated.   This rapid emergence could likely be explained by rapid hepatic metabolism of the propofol as well as residual naltrexone binding of mu opioid receptors decreasing the efficacy of fentanyl.  The patient was transported to the PACU with no evidence of emergence delirium and seemingly in good spirits with good pain control.  However, 30 minutes later the PACU nurse called me to report that she had given an additional 200 mcg of fentanyl in PACU for pain control and the patient was reporting 10/10 pain.  This was unusual in that the small lipoma excision had been anesthetized with local anesthetic.  Hydromorphone was ordered and no more calls were forthcoming.

Currently there is an epidemic occurring in America with opioid abuse.  It is becoming ever more likely that we will be required to care for one of these patients. Many of these patients will require therapy such as suboxone to prevent cravings of opioid.  Suboxone is a combination of buprenorphine and naltrexone where  the ratio is 4 parts buprenorphine to 1 part naltrexone.  The naltrexone is included to prevent the crushing and snorting or intravenous injection and is not considered to be active when suboxone is taken as intended. Buprenorphine is a partial agonist at the mu receptor.  It is also a kappa antagonist. These receptors are predominantly located in the spinal cord.  As a partial agonist, buprenorphine has a ceiling affect which occurs at about 32 mg / day.  Most patients who are on buprenorphine (suboxone) for maintenance therapy, are on doses that are higher than for treatment of chronic pain (i.e 16 mg for maintenance vs 2 to 4 mg for chronic pain therapy). There are two issues that anesthesiologists need to understand when patients arrive for surgery on suboxone.  First is the underlying pharmacokinetics.  Suboxone, if provided as a patch takes a full seven days to clear.  Buprenorphine is also prescribed to be taken sublingual where the bioavailability is  30 to 50%. The half life of high dose buprenorphine (as used for maintenance therapy in opioid dependent patients)  is 20 to 70 hours. However, the half-life is high variable and depends on patient characteristics as well as the dosing regimen. It is clear from case reports that maintaining suboxone in the preoperative period will lead to very poor pain control amid escalating pure mu opioid agonist requirements. For elective surgery, where significant post op pain is anticipated, it is recommended that patients discontinue suboxone therapy for five days.  In urgent/emergent surgical patients presenting on suboxone maintenance therapy, it may be very difficult to override the suboxone from the mu receptor. The reason for this difficulty is a result of the very high affinity for the mu opioid receptor by buprenorphine.  It has been noted that buprenorphine binds the mu receptor avidly, and only slowly diffuses away.  Therefore, the mu receptor remains unavailable to pure mu agonists. Consequently,  respiratory depression is a risk at the very high dosages required to achieve pain control.  It may be wise to titrate a rapid onset opioid (fentanyl) prior to surgery in the operating room to help anticipate what dose the patient may tolerate or require for post op pain control.  Suboxone should not be given during the preoperative period to avoid precipitating additional pain.  For patients where post op pain is anticipated to be minor or mainly controlled via other means (i.e. local anesthetics) suboxone may be continued in the preoperative period.
My patient was on naltrexone.  As a mu antagonist, it was anticipated that override might be difficult.  While, indeed, higher doses of fentanyl than typical were required, the requirements were not extraordinary.  Once again, an understanding of pharmacokinetics is important to determine how difficult it might be to override any naltrexone present at the mu receptor.  A single oral dose of 25 mg of naltrexone has an apparent half-life (t1/2) of 14 hours. Veberey et al. [2], looked at naltrexone effectiveness in blockade of heroin 25 mg. After a 100 mg oral dose of naltrexone, there was 96% blockade at 24 hours, 86.5% blockade at 48 hours, and 46.6% at 72 hours. Therefore, it would seem prudent to recommend that patients avoid naltrexone for 72 hours prior to any surgery where it is anticipated that opioids are going to important to control post op pain.  In patients who have chronically taken naltrexone for maintenance therapy, there is up regulation of mu receptors in the brain [8]. Therefore, patients who discontinue naltrexone, may be resistant or more susceptible to opioids depending on how much naltrexone remains in the system compared to the degree of mu opioid receptor upregulation.  While naltrexone is a mu opioid antangonist, it is approved by the FDA for treatment of alcoholism because it reduces the euphoria and positive reinforcing effects of ethanol use [9].
Lastly, this patient had a history of vitamin B12 deficiency.  Vitamin B12 is an integral part of two biochemical reactions: the conversion of L-methylmalonyl coenzyme A into succinylcholine coenzyme A and the formation of methionine by methylation of homocysteine.  These reactions are critical for the synthesis of DNA and to the maintenance of the myelin sheath by methylation of myelin basic protein. Active Vitamin B12 contains cobalt in its reduced form (Co+).  Nitrous oxide produces irreversible oxidation to the Co++ form leading to inactive Vitamin B12. The result is an irreversible inactivation of the enzyme methionine synthase  There are several case reports in the literature of patients developing subacute combined degeneration of the spinal cord following nitrous oxide anesthesia [11,12,13].  In these case reports, the diagnosis of subacute combined degeneration of the spinal cord was made several weeks post op after otherwise routine and uneventful anesthesia. Subacute combined degeneration of the spinal cord is characterized by degeneration of the posterior and lateral columns.   The avoidance of nitrous oxide in patients with anemia of unknown cause or in patients at risk of vitamin B12 depletion is recommended.   A significant risk factor for Vitamin B12 depletion is alcoholism for two reasons. 1) alcohol abuse leads to poor nutrition and therefore, vitamin B12 intake is reduced, and 2) excessive alcohol use leads to atrophic gastritis.  Atrophic gastritis is characterized by inflammation and dysfunction on the cells lining the stomach so that production and secretion of intrinsic factor is compromised.   Intrinsic Factor (IF) is essential for the absorption of vitamin B12.  Atrophic gastritis also decreases the production of hydrochloric acid. The increase in pH leads to overgrowth of different bacterial strains that consume vitamin B12 and reduction in efficiency of food breakdown leading to the release of vitamin B12.

Lastly, her seizure episode following anesthesia should be addressed more fully in context of her history alcoholism.  While there are case reports of severe vitamin B12 deficiency leading to seizures, this isn't typical.  What  is more common in alcoholics undergoing surgery is alcohol withdrawal syndrome (AWS). AWS can result in an incidence of mortality of around 15% if untreated [14]. In patients who abuse alcohol, AWS more commonly manifests during stress such as surgery [15]. It has been suggested that in operative patients, hypotension, hypoxia, or uncontrolled pain in the PACU may precipitate AWS [16].  The key features of AWS include hyperexcitability of the CNS due to reduced GABA activity and increased glutaminergic action [17]. Increased noradrenergic activity can lead to hypertension, tachycardia, sweating, tremor, and hallucinations.  Lastly, seizures can occur. Seizures typically occur early in the process, i.e. 6 to 8 hours after stopping alcohol intake. This is long before the most severe manifestations of AWS, which may take 3 to 4 days. Attributing this patients prior post anesthetic seizure to AWS may be reasonable, but can't be proven.

In conclusion, this patient had multiple medical issues that were impactful on making an anesthetic plan.  These included a history of seizures related to anesthesia and vitamin b12 depletion, alcoholism treated with naltrexone and prazosin, as well as high anxiety with a  history of severe emergence delirium requiring treatment.  In this patient, using TIVA, local anesthesia for the surgery site, along with a BIS monitor allowed for an uneventful anesthetic and emergence.




1. Lepouse c et al.  Emergence delirium in adults in the post-anesthesia care unit, BJA, 2006, vol. 96(6), 747-53.
2. Verebey K. The clinical pharmacology of naltrexone: pharmacology and pharmacodynamics. NIDA Res Monogr 1981;28: 147-58.
3. Curtis D, Stevens WC. Recovery from general anesthesia. Int. Anesthsiol. Clin, 1991;29(2):1-11.
4. Lovestrand D, Phipps S, and Lovestrand S.  Posttraumatic stress disorder and Anesthesia Emergence.    AANA Journal, 2013(81).3. 199-203.

5. McGhee LL, Maani CV, Garza TH, DeSocio PA, Gaylord KM, Black IH. The relationship of intravenous midazolam and posttraumatic stress disorder development in burned soldiers. J Trauma Inj Infect Crit Care. 2009;66(4 suppl):S186-S190 
6.  Wilson JT, Pokorny ME. Experiences of military CRNAs with ser- vice personnel who are emerging from general anesthesia. AANA J. 2012;80(4):260-265.
7.  McGhee LL, Maani CV, Garza TH, DeSocio PA, Gaylord KM, Black IH. The correlation between ketamine and posttraumatic stress disorder in burned service members. J Trauma Inj Infect Crit Care. 2008;64(2 suppl):S195-S199.
8. Yoburn BC, Luke MC, Pasternak GW, Inturrisi CE. Upregulation of opioid receptor subtypes correlates with potency changes of morphine and DADLE. Life Sciences 1988;43: 1319-24.
9.  Volpicelli JR, Alterman AL, Hayashida M, O'Brien CP. Naltrexone in the treatment of alcohol dependence. Arch Gen Psych 1992;49: 876-80
10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408515/
11. https://www.ncbi.nlm.nih.gov/pubmed/19169627
12.  https://www.ncbi.nlm.nih.gov/pubmed/11455686
13. http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949600
14. http://journals.lww.com/anesthesia-analgesia/Citation/1999/04000/Alcohol_Withdrawal_in_the_Surgical_Patient_.50.aspx
15. C. Spies, H. Tønnesen, S. Andreasson, A. Helander, and K. Conigrave, “Perioperative morbidity and mortality in chronic alcoholic patients,” Alcoholism, vol. 25, no. 5, pp. 164S–170S, 2001. 
16. https://www.hindawi.com/journals/cria/2013/761527/
17. http://search.proquest.com/openview/252f427f24a32c20bff649b85e2cd535/1?pq-origsite=gscholar&cbl=2031130

August 9, 2016

elevated preoperative BNP, what do I do now?

A rather unhealthy and unkept gentleman of about 54 years of age presented to the ER after a 'fall'.  He presented to the preop area as an add for intertrochanteric nail by our friendly orthopedic surgeon.

I was assigned the case and went over to look through the chart.

I noted a cardiology note that indicated that his troponin levels were very slightly elevated and an echocardiogram was recommended by the cardiology NP. Since this gentleman, had an injury that was better treated sooner than later (more discussion on this below), and he did not have an EKG with any indication of ischemia, I was not convinced that delaying his surgery for an additional day to perform an echo was absolutely required.  I continued to look for more information to determine the liklihood that an his slight bump in troponins represented something truly sinister, or was perhaps more benign in nature.  It was known that he was likely homeless, dehydrated, and had a mild elevation in his BUN and creatinine consistent with pre renal azotemia in a dehydrated (hypovolemia) patient.

A further review of his chart revealed that he also had a BNP of over 1200 pg and lasix had been ordered by the ER physician, but not yet administered due to various logistical issues.  At this point, I decided to call the Ortho surgeon and have a conversation with him.  After discussing it with him, a decision was made to cancel the surgery until his volume level could be better determined, and optimized.
Patients in heart failure are poor candidates for surgery.  Post operative morbidity and mortality is significantly higher; and any elective surgery is contraindicated when if patients are in failure.  is predictor of poor outcome in non cardiac surgery.  Typically, it is best to post pone non emergent surgery in patients suspected or known to be in hear failure.  Unfortunately, clinical signs of heart failure (dyspnea, jugular vein distention, leg swelling etc) are not perfect indicators of a patient's status.  Current evidence suggests that hip fracture patients have better outcomes when the fracture is repaired within 24 hours of admission.  Therefore, an anesthesiologist who makes a decision to delay hip fracture surgery may potentially increase overall  risk to the patient in an attempt to improve the patients perceived short term risks.

Atrial Natriuretic Peptide (ANP) was originally isolated from rat atrial myocardium. In humans, it is secreted predominantly by atrial myocytes.  BNP was subsequently isolated from porcine brains. In humans it is secreted by both atrial and ventricular myocytes, but it is predominantly the ventricular myocytes that secrete BNP. These natriuretic peptides have several functions in normal physiology. When cardiac myocytes are stretched due to increased load or volume, secretion of these peptides results in: 1) down regulation of the sympathetic nervous system, and the renin-angiotensin-aldosterone system, 2) improved natriuresis and diuresis via afferent and efferent hemodynamic mechanisms of the distal tubule of the kidney, 3) decreasing peripheral vascular resistance via relaxation of smooth muscle. A BNP precursor is secreted by left ventricular myocytes which is synthesized into proBNP.  This short lived molecule is cleaved into the biologically active C terminal portion and biologically inactive N-terminal (NT-proBNP) portion.

In a observational study, BNP was found to be an independent predictor of increased cardiac events after non cardiac surgery and performed better than a preoperative scoring system after abdominal surgery [1].
It is known that BNP levels correlate with demodynamic parameters such as right atrial pressure, PCWP, and left ventricular end diastolic pressures.   Echo studies looking at the correlation of BNP levels with ventricular function have also been done.  Usuing the NYHA classificaiton system we find that in class I, BNP averages 240 pg, II 390 pg, III; 640 pg and IV 820 pg.  This indicates that higher levels do seem to correlate with more significant cardiac dysfunction.

In 2002, the national breathing not properly (BNP) trial was completed and was able to show that plasma BNP measurement was able to differentiate between CHF  and non CHF causes of dyspnea (area under receiver operating characteristic curve = 0.91) [2]. In this trial, a single BNP measurement was also more accurate than two commonly used methods of determining cardiac causes of SOB, the National Health and Nutritional Examination score and Franghiham (see below).


Using data from this same study, a patient presenting with SOB, and a BNP less than 50 pg/mL has an 7% chance that the cause is heart failure. If the BNP is between 50 pg/mL and 150 pg/mL, the chance that heart failure is the causes rises to 36%.  With a BNP of greater than 150 pg/mL, there is an 83% chance of heart failure. Later, another study concluded that if the BNP level was less than 100 pg/mL, there was a low liklihood for congestive heart failure.  Alternatively, in this study, they concluded that blood levels greater than 500 pg/mL made a diagnosis of heart failure extremely likely [3].

In another smaller study, dao et al. showed that a BNP of less than 80 pg/mL had a 98% negative predictive value. In this same trial, patients  with dyspnea and diagnosed with CHF had a mean BNP of 1076 pg/mL while patients who had dyspnea but were found not to be in heart failure had a mean BNP of only 38 pg/mL.  
A study of patients undergoing non cardiac surgery found that an elevated BNP measurement was an independent predictor of postoperative cardiac events. In this study, BNP measurements outperformed the goldman multifactorial clinical index in predicting cardiac adverse events after non cardiac surgery.  (fee figures below for a great summary of this study).





They showed that a BNP level of 0 to 100 pg/mL had zero risk,  BNP levels of 201-300 pg/mL was considered low risk (5% event rate),  intermediate risk (12% event rate) was from 200 to 300 pg/mL, and high risk (greater than 300 pg/mL) had an event rate of 81% [4]. This was followed up with another study that was able to demonstrate that BNP levels greater than 40 pg/mL was associated with a seven fold increase in cardiac events in the early post operative period and longer hospital stay [5]. Yeh et al. found that pre operative NT pro-BNP independently predicted cardiac complications in non cardiac surgery (greater than 450 ng/L) with 100% sensitivity and 83% specificy [6].

The clinician should recognize that there are several causes other than heart failure that can result in elevated BNP levels.  These include renal failure (decreased clearance), pulmonary embolism, pulmonary hypertension, and chronic hypoxia.  Furthermore, BNP increases along with age. A trial was able to determine five independent predictors of elevated BNP in patients without heart failure.  They were 1) low hemoglobin values, 2) low BMI, 3) history of A fib 4) radiographic cardiomegaly, and 5) advanced age. This is why this test has been found to have very good sensitivity, but not great specificity.  Put another way, if the BNP is normal, the clinician has very high confidence that the patient is not currently in CHF or that cardiac complications will be low.  However, the opposite is not true; if the BNP is elevated, the clinician cannot be as confident that the case should be cancelled or delayed because of certain CHF in the patient.  However, ruling out the above other causes of elevated BNP can aid the clinician in ruling out other sources of an elevated BNP.

BNP also tracks appropriate therapy.  Therefore, patients being treated with ACE inhibitors and diuretics will have lower than typical BNP levels, while other medications may increase BNP (beta blockers and digoxin).

Unfortunately, at this point, rigorous testing in the preoperative setting to determine cut off points for BNP levels in order to determine whether cases should be cancelled or not have not been done.  In "up to date" the following quote relays the current recommendations regarding the use of BNP in the preoperative period to aid in evaluation of the patient: "However, it is unknown whether or which changes in perioperative management would improve outcomes in surgical patients with elevated BNP or NT-proBNP levels".

Determining when to delay or cancel hip fracture surgery is often a challenge for the anesthesiologist. Particularly since this population of patients generally have significant co morbidities that would result in cancelation or delay in purely elective surgery.  Orthopedists are becoming more aggressive in trying to bring their patients to surgery within 24 hours of injury because of numerous observational trials indicating that early hip fracture surgical repair leads to better functional outcome and lower rates of complications and mortality. In fact, current guidelines recommend surgery within 24 hours of injury [6].  Early surgery has also been included as a quality marker in the highly disseminated set of Inpatient Quality Indicators from the Agency for Healthcare Research and Quality [7].  So, would my patient be better off, overall,  if I had administered lasix in the holding area, and proceeded to surgery within the next 30 minutes to hour?
Observational trials are prone to selection bias, attrition and detection bias.  Prospective observational trials are more robust generally than retrospective trials, but a recent systematic review found that currently, 65% of studies addressing this issue are retrospective, and therefore, subject to confounding and biased ascertainment of outcomes. One of the most obvious problems with retrospective observational trials is that patient who are sicker are more likely to be delayed and therefore, have a larger time delay between the injury and the surgery.  Therefore, it is likely that patients will have better outcomes in the 'early' surgery group vs. the later surgery group because the early surgery group is a healthier cohort.  As an example, a recent large [8] retrospective observational trial in Spain looked at over 81,000 patients who had hip fracture surgery.  They found a positive correlation with early surgery and lower in hospital mortality.  However, after correcting for a multitude of variables, they found that indeed, patients at much higher risk had delayed surgery, and after correcting for this, there was no longer any effect on mortality from delaying surgery.  In another study, the authors were able to demonstrate that individualizing the timing of surgery to medically optimize patients at higher risk led to improved outcomes [9]. Vidan et al. and Khan et al also showed that when controlling for medical co-morbidities, timing of surgery ceased to be a factor in mortality difference between groups [10,11]. Still, while it seems difficult to say that mortality is improved with early surgery after injury (within 24 hours), other important metrics may be apt for improvement.  Investigators have found that time to discharge was 10.9 days earlier  if surgery is performed within 48 hours [12], and another study concluded that surgery within 24 hours decreased LOS by 4 days [13].  Other clinically relevant benefits found with early surgery include a decrease in the incidence of decubitus ulcer formation and an increased likelihood of return to independent living.
In summary, at this point, due to lack of prospective RCTs, it is not clear that early surgery (within 24 to 48 hours of injury) can reduce mortality.  However, other parameters, such as LOS, pressure ulcer formation and long term functional recovery may be improved by early surgery.  While guidelines recommend that patients go to the OR for operative repair within 24 to 48 hours of injury, the anesthesiologist should feel confident that a delay in surgery to allow for medical optimization of severe evolving medical conditions is warranted.  Each case should be judged by its own merits and the anesthesiologists should play a role in not obstructing early surgery unless truly necessary. As an example, I recently reported on a case where a patient with a hip fracture was admitted for operative repair, but the gastroenterologist recommended a transfer because the patient had severe liver dysfunction.  The orthopedist called me and I recommended proceeding with surgery given the enormous delay caused by a transfer and lack of evidence that further optimization could improve the patients outcome.  This case proceeded as scheduled, although, the gastroenterologist, inked in the chart that he recommended a spinal which created a medico legal issue for the anesthesiologist.



1. Mercantini P, et al. Preoperative brain natriuretic peptide (BNP) is a better predictor of adverse cardiac events compared to preoperative scoring system in patients who underwent abdominal surgery.  World J Surg 2012 Jan;36(1):24-30.
2. Maisel AM, Krishnaswamy P, Nowak R, et al. Bedside B-type natriuretic peptide in the emergency diagnosis of heart failure: primary results from the Breathing Not Properly (BNP) Multinational study. Paper presented at: 51st Annual Scientific Session of the American College of Cardiology;March 17–20,2002; Atlanta, Ga.


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    July 25, 2016

    cysto after laparoscopic surgery to verify ureter patency

    A 37 year old female presented for diag laparoscopy for suspected ectopic pregnancy and mass in the left adnexa.

    The procedure was uneventful, however, the surgeon was unable to visualize the ureters after performing a left salpingectomy.  She was concerned about the ureters enough to perform a post operative cystoscopy to verify that both ureters remained functional.  We verified that the only dye available to us was indocyanine green and methylene blue.   I was given methylene blue and injected 3 1/2  mLs.  After 20 minutes, no visible dye appeared in the bladder and the procedure was terminated with the plan to follow carefully her course.

    There are three common dyes that anesthesiologist are asked to inject patients in order for diagnostic purposes.  The anesthesiologist should have familiarity with the properties of any medication they inject.  A review of information on these dyes revealed a deficit in my own knowledge in this regard.

    Methylene Blue can be used to test ureteral patency after laparoscopic surgery.  However, it is not commonly used for this indication.  The recommended dose is 50 mg (it comes as a 10mg/mL concentration) for this purpose.  Methylene blue does not have FDA approval for this use, and the package insert only asserts its use as a treatment for methemoglobinemia.

    Methylene blue is the only medication known to be effective for the treatment of methemoglobinemia, which is the oxidation of the iron in hemoglobin to the ferric form.  Normally, the blood has a 1% concentration of methemoglobin (hemoglobin in the ferric form).  When the concentration of methemoglobin rises to about 15%, symptoms become apparent and require treatment.  The negative effects of this disorder result from hypoxia, as oxygen cannot be efficiently carried by methemoglobin.  Symptoms include ashen color skin or cyanosis (methemoglobin from 3 to 20%), headache, dyspnea, lightheadedness (up to 50%), arrhythmias, unconsciousness etc (greater than 50% methemoglobin level).  Treatment dose of methylene blue is 1 mg to 2 mg/kg.  Ironically, at doses greater than 7 mg/kg can lead to the inducement of methemoglobinemia.

    Methylene blue inhibits monoamine oxidase enzyme, and therefore, can result in serotonin syndrome and should be used if with caution in patients taking serotonin reuptake inhibitors or MAO inhibitors.

    As methylene blue can be used for verification of ureteral patency via cystoscopy as the urine should turn blue after 10 to 20 min of IV injection, I thought it curious that we had no evidence of blue urine after 30 min.  However, joel et al. did publish a look at two cases where injection of methylene blue did not result in any change in urine color [1].  The authors suspected that rapid metabolism of methylene blue to leulomethylene (a colorless metabolite was the cause of this anomaly).  Since indigo carmine does not undergo any metabolism prior to excretion into the urine, it would be a superior alternative to methylene blue for detection of ureteral patency using cystoscopy.  Indigo carmine's package insert asserts its primary use is for detecting change in urine color after IV injection.  There are no drug interactions with indigo carmine, making it a safer alternative as well. The dose recommended is the full 5  mL ampule.

    Indocyanine Green is another dye that may be encountered.  It's used for determination of cardiac output, hepatic function and ophthalmic angiography (5mg, 0.5 mg/kg, and 40 mg respectively).  It is bound to plasma proteins and taken up by hepatocytes without metabolism, and secreted in the bile unchanged.  There are reports of the use of indocyanine green to detect ureteral patency via cystoscopy, however, it has been reported to be used in robotic surgery to detect ureters with near infrared light with success.  However, the dye was injected directly into the ureters.  Recently, I was involved in a case where a patient had an internal hernia with small bowel strangulation leading to questionable viability of the small bowel. Indocyanine green was injection IV and a laser was used to evaluate blood flow and vascular patency to the bowel.  This technique is known as laser florescence angiography and uses the florescence properties of indocyanine green to visualize vessels that need to be verified as patent.  With the laser set in place, the room lights off, an injection of indocyanine green is given IV, and within a few moments, the area of interest should light up white on the proper viewing screen where vessels are patent.  Using this technique, we the surgeons were quickly able to verify that all vessels to the bowel section of interest were patent.

    Anesthesiologists are often asked to inject substances that lie outside our typical armamentarium.  We have an obligation to understand the possible ramifications of what we inject, and not always assume that it is proper and safe.





    Joel AB, Mueller MD, Pahira JJ, Mordkin RM. Nonvisualization of intravenous methylene blue in patients with clinically normal renal function. Urology 2001; 58: 607vii. - See more at: http://www.ashp.org/menu/DrugShortages/CurrentShortages/Bulletin.aspx?id=27#sthash.ado1taUN.dpuf

    July 7, 2016

    end tidal CO2, what intraoperative role can it play?

    Today I had a 64 year old male, with no reported medical history, who presented for L4-5 laminectomy.  The patient reported that he walked regularly, up to 2 miles with no history of SOB, chest pain or other symptoms.  The patient was taken to the OR and given 2 mg versed, 100 mcg fentanyl, 180 mg propofol, 5 mg rocuronium, and 100 mg succinylcholine.  IV decadron was also given (8mg).  Intubation proceeded without event and the patient was placed in the prone position.  After turning prone, several issues arose at the same time.  First, pulse oximetry revealed 93% saturation.  Simultaneously, the blood pressure read 50/20 mmHg. ECG appeared normal with SR at 74 bpm.  The pulse plethysmograph waveform appeared robust without obvious issues aberrations.
    Ausculation of the lungs was challenging due to a large tissue mass making breath sounds difficult to detect.  However, it was noted by myself, that there appeared to be no breath sounds on the left, and therefore, the ETT was pulled back slightly.  This resulted in an improvement of the arterial saturation as measured by pulse oximetry.  However, simultaneous troubleshooting of the significant apparent hypotension occurred.  The blood pressure cuff was recycled, and low blood pressure was verified.  Also of note, the capnogram was reading 20 mmHg.  The patient was noted to be ventilated at 700 mL with RR of 10.  The patient weighed approximately 100 to 105 kg. It was immediately apparent that elevated minute ventilation was not likely the sole contributor to the issues related to the hypocapnea.

    While multiple issues were at play at once in this case (endobronchial intubation along with severe hypotension), a deeper exploration of how the capnogram can be helpful in the diagnosis of the issues  at hand.

    In general, end tidal carbon dioxide (etCO2), is a function of PaCO2.  However, a multitude of parameters can cause a gap (this is dead space [Vd], written as (a-ET)PCO2).  In general, healthy patients without significant lung disease will have up to a 5 mmHg difference, where the etCO2 will be less than actual measure PaCO2.    This gap increases with age, emphysema or any state that increass dead space ventilation (Vd), like low cardiac output (from hypovolemia) or pulmonary embolism.  On the other hand, (a-ET)PCO2 can actually be positive (i.e. etCO2 is greater than PaCO2) in pregnancy and children (from 1 to 3 mmHg). In general clinical practice, we do not have access to the (a-ET)PCO2 because we do not routinely measure arterial blood gases.  However, we do follow the trend of the etCO2, and thus, in general, if we see a sudden decrease in the etCO2 on the capnogram, we assume that we may be hyperventilating the patient, or that there has been a sudden increase in dead space ventilation.  However, it must be understood, that there are several parameters other than Vd that can cause a decrease in etCO2. For example, decrease in metabolism or VCO2 will result in decrease in etCO2 if minute ventilation is constant. VCO2 is a function of depth of anesthesia relative to surgical stimulus, and body temperature.  Alternatively, an increase in minute ventilation, if metabolic rate is constant will cause etCO2 to decrease.  Importantly, the (a-ET)PC02, will remain the same in the two above situations.  Another, more sutbtle and less recognized mechanism for (a-ET)PCO2 to be affected is via FiO2.  Yamauchi et al. demonstrated that increasing the FiO2 from room air to very high caused an ever increasing (a-ET)PCO2. [8] They found that Vd increased as the FiO2 was increased in their anesthetized patients.  They presumed that the mechanism of the increase in Vd was an increase in pulmonary vascular dilation with increased oxygen tension.  This occurs predominantly in highly perfused alveolar units resulting in a shunt of blood away from low perfused alveolar units to high perfused alveolar units.  Of course, this shunt created from increasing FiO2 is not related to physiologic shunts that might occur with something like ARDS.  In this case, only large shunts of greater than 30 to 40% will cause a significant change in the (a-ET)PCO2.

    However, a state of low cardiac output can also result in a reduced pulmonary artery blood flow. This results in increased Vd, and thus the (a-ET)PC02 increases.  This manifests in the operating room as a sudden decrease of etCO2.  This pattern was looked at by Askrog and colleagues where an inverse linear correlation was found between pulmonary artery pressure and (a-ET)PCO2. [1]     Things that can cause this include pulmonary emboli (air, debris, clots), sudden massive hemorrhage leading to reduced venous blood return, vasodilation, mechanical obstruction to blood flow, reduced cardiac contractility, etc.  In general, in the OR, mechanical ventilation and anesthetic depth are maintained at a reasonably constant level allowing us to remove these as a cause in theory.

    In my patient, the simultaneous low blood pressure and sudden drop in etCO2, indicated two things: the blood pressure was real (i.e. it was not artifactual), and the drop in etCO2 was most likely due to decreased CO, in this case  the cause being overdose of anesthesia. Of course other causes of a precipitous drop in etCO2 include PE or other mechanical obstruction to pulmonary blood flow.  As it turns out the percent decrease in etCO2 is directly correlated with the percent decrease in CO (assuming that the metabolic rate and alveolar ventilation are unchanged). This was demonstrated in an article published in A and A. [2]  It should be noted that after sustained or constant low CO, (i.e. after 10 to 20 min) CO2 begins to accumulate in the peripheral tissues leading to an increase in CO2 delivery to the pulmonary vasculature.  This will cause the etCO2 to return to baseline if all other factors remain unchanged.  The relationship of etCO2 and pulmonary blood flow was also studied in patients coming off cardiopulmonary bypass. [3]  Here, an etCO2 greater than 30 mmHg (the study did not include patients with significant lung disease), was associated with CO of greater than 4 L/min (CI of 2 L/m). When etCO2 was greater than 34 mmHg, pulmonary blood flow (a good surrogate for CO) was greater than 5 L/min. Once again, minute ventilation was carefully maintained.
    Recently, a large volume of literature has been produced looking at measurements of indices that indicate a patient who is hypovolemic. Pulse pressure variation and stroke volume variation via measurement and analysis of the arterial waveform in ventilated patients in sinus rhythm has proven effective at determing which patients are likely going to respond with increased cardiac output if a fluid bolus is given.  Unfortunately, the equipment is costly, requires a fair amount of data input, and is usually not routinely available. Recently, Monnet et al. [4] was able to show that etCO2 was better than arterial pressure for predicting volume responsiveness when using a passive leg raising test. Using a similar methodology in patients with acute circulatory failure in the ICU, monge garcia et al. showed that etCO2 after passive leg raise maneuver could be used to track changes in CO  for the prediction of fluid responsiveness. [5]  Recently, a group in France was able to demonstrate that after 500 mL hetastarch, an increasae of 2 mmHg in the etCO2 could diagnose fluid responsiveness (specificity 98%, sensitivity 60%). Obviously, it is critical to undertand that other changes to CO2 production and elimination must be held constant for this to be a valid clinical indicator.  It should be recognized that in clinical anesthesia this can be difficult.  In fact, very recently, I took care of patient having an open partial colectomy with small bowell resection.  Her BP trailed lower early in the case.  Based on this article, I decided to carefully track etCO2 and maintain other parameters unchanged (i.e. CO2 production and minute ventilation).  I quickly boluses in 500 mL of hetastarch as used in the above mentioned article.  While I did notice that etCO2 trailed higher with this bolus, I realized that in clinical practice, there are so many other factors occurring that it can be challenging to feel confident that other parameters are not the cause of the change you see reading on the capnogram.   However, importantly,  in this same study, HR variation, MAP variation, and PP variation were not predictive of volume responsiveness. In summary, these authors showed that after a rapid infusion of 500 mL colloid, an increase of 5.8% (or about 2 mmHg) of etCO2 predicted fluid responsiveness in 100% of their patients.  If the etCO2 increased less than 5.8%, no conclusions could be drawn. [6]  In real clinical practice, a bolus must be given very rapidly, to ensure that other parameters don't account for any subtle changes seen on the etCO2.
    Others have demonstrated that etCO2 can be predictive of mortality after out of hospital cardiac arrest (OHCA). In the NEJM [7], an observational study was published looking at etCO2 monitoring following OHCA to determine effectiveness of ACLS.  They found that in this patient population, if  after 20 minutes of ACLS, the etCO2 was less than 10 mmHg, there was a 100% specificity and specificity to determine non survival to hospital admission.  If the etCO2 was greater than 20 mmHg, this indicates survival (at least in this study), but it does not guarantee it.  In this article, it was noted that in low flow states (i.e. low cardiac output), etCO2 becomes a much better surrogate for cardiac output.

    Having an in depth understanding of etCO2 can help us in ways that we might not otherwise expect.





    [1]  Askrog V.  Changes in  (a-A)CO2 difference and pulmonary artery pressure in anesthetized man. J Appl Physiol 1966;;21:1299-1305.
    [2] Shibutani K, Muraoka M, Shirasaki S, Kabul K, Sanchala VT, Gupte P.  Do changes in end-tidal PCO2 quantitatively reflect changes in cardiac output? Anesth Analg 1994;79:829-33.
    [3] Maslow A, Stearns G, Bert A, Feng W, Price D, Schwartz C, Mackinnon S, Rotenberg F, Hopkins R, Cooper G, Singh A, Loring SH. Monitoring end-tidal carbon dioxide during weaning from cardiopulmonary bypass in patients without significant lung disease. Anesth Analg 2001;92:306-13.
    [4] Monnet X, Bataille A, Magalhaes E, Barrois J, Le Corre M, Gosset C, Guerin L, Richard C, Teboul J-L. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test. Intensive Care Med 2013;39: 93–100. 
    [5] Monge García MI, Gil Cano A, Gracia Romero M, Monterroso Pintado R, Pérez Madueño V, Díaz Monrové JC. Non-invasive assessment of fluid responsiveness by changes in partial end-tidal CO2 pressure during a passive leg-raising maneuver. Ann Intensive Care. 2012;2:9
    [6] Jacquet-Lagreze M, baudin F, David JS, Fellahi JL, Hu PB, Lilot Ma, Piriou V. End -tidal carbond dioxide variation after a 100- and a 500-ml fluid challenge to assess fluid responsiveness.  Annals of Intensive Care 2016 6:37.
    [7]Levine R, et al. End Tidal Carbon Dioxide and Outcome of Out-of-Hospital Cardiac Arrest. NEJM; 337(5):301.
    [8] Yamauchi H, Ito S, Sasano H, Azami T, Fisher T, Sobue K.  Dependence of the gradient between arterial and end-tidal PCO2 on the fraction of inspired oxygen.  BJA. 2011.107(4):631-5.

    June 8, 2016

    Liver cirrhosis and hip fracture

    A few days ago our friendly orthopedic  surgeon posted case for IM nail in a hip fracture patient who was 73 years old.  Unfortunately, the patient had long standing cirrhosis secondary to hepatitis C, with complications related to his cirrhosis of portal hypertension and grade I varices, encephalopathy, thrombocytopenia and elevated INR.  The consultant GI doctor told the Orthopedic surgeon that this patient should not have hip fracture surgery at our community hospital due to high mortality due to his Childs Pugh classification.  The orthopedic surgeon asked the consultant GI doc if it would be ok to do the surgery under spinal.  The GI doc said that would be fine and therefore, the surgeon called me to ask if my anesthesia practice could do a spinal.

    The Child-Pugh score considers the patients bilirubin, albumin, INR, presence or absence of encephalopathy, and presence or absence of ascites.  In this patient prior to surgery his breakdown was as follows:

    Bilirubin: 4.2 mg/dl (greater than 3 mg/dl = 3 pts)
    Albumin: 2.4 g/dl (<2 .8="" dl="3" g="" p="" pts="">INR:  1.4  (<1 .7="1" p="" pt="">No ascites = 1 pt
    encephalopathy (medically controlled) = 2 pts

    His total score is 10 pts which makes him a grade C.  Life expectancy is 1 to 3 years and mortality with major abdominal surgery is 82%.  Obviously, preoperative mortality in these patients is extreme, making elective surgery an unlikely choice.  However, this was essentially urgent life potentially life saving surgery, and furthermore, was not major abdominal, but an IM nail.


    Child-Pugh Calculations


    Points*
    123
    *CTP score is obtained by adding the score for each parameter.
    CTP class:
    A = 5-6 points (predicted mortality major abdominal surgery ~10%)
    <5 p="">B = 7-9 points (predicted mortality major abdominal surgery- ~25%)
    C = 10-15 points (predicted mortality major abdominal surgery greater than 50%)

    Making a determination of the severity of a patient's liver disease is a challenging problem.  It is important to quickly classify a patient presenting for surgery as compensated liver cirrhosis or decompensated cirrhosis.

    Compensated cirrhosis is a patient that does not have ascites, jaundice, encephalopathy, or variceal bleeding.  If any of these are present, it is considered decompensated cirrhosis.   In patients with compensated cirrhosis, the Child-Pugh classification can be a good guide to the severity of their disease.  A Recent systemic review found the Child-Pugh score was still significant among the predictors of death despite the absence of ascites, encephalopathy and jaundice in the patients with compensated cirrhosis, because its laboratory components, bilirubin, albumin and prothrombin time continued to be among the most frequent predictors, indicating that even subtle abnormalities in these laboratory parameters are predictive of death [1]. The Child-Pugh score was originally designed about 30 years ago to predict mortality with surgery for portal hypertension.  Since this time, the MELD score was created to predict the mortality following a transjugular intrahepatic shunt procedure (TIPS). Later it was adapted to risk stratify patients on the waiting list for liver transplantation. The MELD score, in addition to considering the INR, bilirubin, and albumin, considers the patients creatinine which is highly correlated with morbidity. Another smaller study in hip arthroplasty patients stated the following, " Of the twelve variables evaluated in our series, a high level of creatinine was found to be the only risk factor associated with perioperative mortality. However, combining all of the categories included in the Child-Pugh scoring system, a higher Child-Pugh score was another important risk factor of perioperative morbidity. " [2]  Therefore, when using the child-Pugh score to evaluated potential risk in a patient, looking for creatinine greater than 1.5 mg/dL is advisable as it likely contributes significantly to overall mortality.

    Even better, however, may be using an online calculator to determine the MELD score. The MELD score has the advantages of  objectivity,  weighing of the variables, and does not rely on arbitrary cutoff values as in the case of the Child-Pugh score. Each one-point increase in the MELD score makes an incremental contribution to risk, thereby suggesting that the MELD score increases precision in predicting postoperative mortality.  Here is a link to a web based calculator (save it as an icon on your phone for ease of use). 
    More recently, studies have tried to determine how the MELD score can predict risk associated with other types of surgery.  In 2005, a retrospective review of 140 patients undergoing surgery found that with a MELD score of 5 to 20, there was a 1% increase in mortality per MELD point increase.   After 20, the risk of mortality increased 2% for each point increase in the MELD score. [4] In this study, they looked at 30 day mortality after surgery, with a 5% mortality rate with a  MELD of 5 pts.  A larger study, also retrospective, found that with a MELD less than 7, the mortality rate was 5.7%.  A MELD score of 8 to 11 increased the mortality rate to 10.3% and with a MELD of 12 to 15 had a mortality rate of 25%.  [5] This was a review with open abdominal, orthopedic and cardiovascular surgery.


    A significant issue related to anesthesia is increased intrapulmonary shunting that can occur resulting in low oxygen saturation.  If significant, this can lead to hepatopulmonary syndrome (HPS). This diagnosis typically requires a saline bubble test using echocardiography where agitated saline is injected IV.  These patients will have dyspnea and hypoxemia when sitting upright, which is relieved by lying flat (orthodeoxia). [3] While this may seem to be of benefit to us since we require the patient be in the supine position these patients tend to be very sick and thus any elective case should be postponed for further evaluation. 

    The key to an anesthetic in a patient with significant cirrhosis who is compensated, is to avoid moving to a decompensated state.  Since these patients often have portal hypertension (portal vein pressure greater than 10 mmHg), blood flow is often very dependent on the hepatic artery and thus MAP. Since all anesthetics (general or spinal) can reduce MAP, hepatic artery blood flow is reduced, and the liver is at risk.  This risk is increased dramatically in abdominal surgery, particularly with laparoscopy where pressure is increased intraperitoneally while MAP is decreased. In advanced cirrhotic liver disease this vulnerability to anesthetics is greatly enhanced due to pathophysiological changes that accompany worsening liver disease.  This can include a decrease in the effective circulating  plasma volume due to several factors: 1) increase in splanchnic blood pooling as a result of increased resistance of blood flow through the cirrhotic liver and 2) vasodilation of the systemic and splanchnic circulation from increased production of vasodilators.  The baroreceptors sense a decrease "load" and thus the SNS, the renin-angiotensin-aldosterone system (RAAS), are activated resulting in significant vasoconstriction in other parts of the body.  Furthermore, a non osmotic release of vasopressin occurs, further enhancing water retention and vasoconstriction.  The end result of all of the forces of hepatic cirrhosis with significant liver congestion, is a state of increased cardiac output, decreased SVR, hypotension, but potentially intense vasoconstriction of renal arteries. It has been demonstrated that as the liver disease progresses, splanchnic vessel vasocodilation increases, and this correlates directly with the low SVR, hyperdynamic state of liver failure with cirrhosis.  It can also be demonstrated that femoral artery and upper extremity arterial flow decreases in sync with increased renal artery vasoconstriction and flow.  The primary cause of this is unclear, but studies suggest that the renal sympathetic system plays a contributory role in renal vasoconstriction in the face of mesenteric vasodilation. What is clear from the work done in animal and human models, is that as the cirrhotic liver worsens, there is a larger impact on blood pooling and vasodilation of the mesenteric vasculature which is the primary culprit in the worsening low SVR hyperdynamic state known to accompany advanced liver cirrhosis.  As this progresses, renal sympathetic tone increases, leading to greater and greater renal artery vasoconstriction until it manifests itself clinically as hepatorenal syndrome, a harbinger of death for most liver patients.

    Therefore, renal function is very important to evaluate prior to anesthesia in patients with advanced liver disease (i.e Child-pugh of Bor C, or MELD score greater than 9 or so).  If new onset elevation in creatinine is noted, this should prompt an immediate renal consult for further evaluation prior to any anesthetic.  Hepatorenal syndrome, can be type 1 or 2.  Type 1 is defined by a doubling of serum creatinine to greater than 2.5 mg/dl in less than two weeks, whereas type 2 develops slowly with creatinine rising to greater than 1.5 mg/dl over time.  HRS type 1 carries a mortality as high a 80% after two weeks. Unfortunately, the diagnosis is one of exclusion, and there are a myriad of other reasons the cirrhotic patient may have renal dysfunction.  In fact, Watt et al. found that only 59% of ARF that was diagnosed as HRS actually fulfilled criteria for the diagnosis, suggesting that HRS is over diagnosed by a large margin.  Having a familiarity with the major criteria is helpful and so I've listed them below:
    MAJOR CRITERIA:

      • Low GFR (i.e. serum creatinine greater than 1.5 mg/dl or 24h creatinine clearance < 40 ml/min).
      • absence of shock, ongoing bacterial infection, fluid losses (i.e. diuretics, diarrehea etc), or treatment with nephrotoxic drugs
      • no sustained improvement in renal function after diuretic withdrawal and expansion of plasma volume with 1.5L of a plasma expander.
      • proteinuria <500 and="" d="" disease.="" evidence="" mg="" no="" obstructive="" of="" or="" parenchymal="" renal="" span="" uropathy="" us="">
    In our case, an elderly male with a child's class C score, if HRS was diagnosed, proceeding with surgery would likely be futile.  Although hip fracture surgery can be lifesaving, and therefore, is not really considered elective surgery, if a the patient goes into this surgery with a diagnosis of HRS type 1, you are most likely putting a patient through a painful, costly operation, with virtually 100% probability of death. 

    As desribed above, two phsyicians (the orthopedic surgeon and the GI doc) formulated an independent anesthesia plan and then decided that was best.  As consultant anesthesiologists, it is important to effective communicate the need to consider a variety of issues that the anesthesiologist may best suited to consider. The reality is that for hip fracture surgery, spinal anesthesia is a great choice, but not for the reasonas assumed by the two physicians.  Spinal anesthesia can impair hepatic artery blood flow as much or more than GETA.  Furthermore, these patients are at particular risk for coagulopathy.  In patients with low SVR and hypotension, spinal anesthesia may not be tolerated well at all.  The reality in our case, was that any anesthesia, spinal or general carried significant risk, but in a patient who did NOT have decompensated liver cirrhosis, it was most prudent to keep the patient and operate as soon as possible for the best possible outcome.

    1. D'Amico G, Garcia-Tsao G, Pagliaro L. Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies. J Hepatol. 2006;44:217–231.
    2. Park YS et al. Perioperative Risk of Hip Arthroplasty in Patients with Cirrhotic Liver Disease. J Korean Med Sci. 2007 Apr; 22(2): 223–226

    3. Wiklund RA Preoperative preparation of patients with advanced liver diseaseCrit Care Med 2004;32:S106-15.
    4.  Northup PG et al. Model for End Stage Liver Disease (MELD) predicts non transplant surgical mortality in patients with cirrhosis. Ann Surg. 2005 Aug; 242(2):244-51
    5. Teh  SH et al. Risk factors for Mortality after surgery in patients with Cirrhosis.  Gastroenterology. 2007 APR; 132(4):1261-9.

    EncephalopathyNoneGrade 1-2
    (or precipitant-induced)
    Grade 3-4
    (or chronic)
    AscitesNoneMild/Moderate
    (diuretic-responsive)
    Severe
    (diuretic-refractory)
    Bilirubin (mg/dL)<2 td="">2-3greater than 3