lets talk about gastroparesis

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caligas

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Are we underapreciating it ask a risk for aspiration? Do you ask additional screening questions to diabetics? Might these patients have gastric contents 8, 10, 12 hours after a meal?

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Gastroparesis is a chronic disorder characterized by impaired gastric emptying and altered motility in the upper GI tract in the absence of mechanical obstruction. It is estimated to affect approximately 5 million individuals in the USA and is most often seen in young individuals with a mean age of onset of 34 years. There is a large female-to-male predominance (4:1 ratio), and gastroparesis is frequently seen in diabetics.[1] It generally presents with nonspecific symptoms including early satiation, nausea, emesis, bloating, abdominal pain, heartburn, anorexia and weight loss. Gastroparesis is likely a heterogeneous condition with the most common etiologies having been identified as idiopathic (36%) and diabetes mellitus (30%).[2] Numerous physiological factors may contribute to symptoms such as abnormalities in liquid and solid meal emptying, emptying of indigestible objects (e.g., fiber), and gastric and proximal small bowel contractility.

The pathophysiology behind gastroparesis is varied and depends upon the etiology of disease. Vagal and/or autonomic neuropathy[3,4] play an important role in the development of diabetic gastroparesis and it is estimated to occur in up to 20–40% of patients with diabetes mellitus.[5] Metabolic abnormalities, especially hyperglycemia, may lead to a delay in gastric emptying, even in healthy individuals.[6] Interruption of hormonal and neural feedback mechanisms is also believed to be significant in the pathogenesis of gastroparesis. The main hormones involved include cholecystokinin from the proximal small bowel as well as glucagon-like peptide-1 (GLP-1), peptide YY from the distal small bowel and amylin from the pancreas.[7] In addition, there is a loss of expression of neuronal nitric oxide, a loss of enteric neurons, smooth muscle abnormalities and disruption of the network of the interstitial cells of Cajal.[8] This can lead to impaired meal-induced relaxation of the gastric fundus, altered intragastric distribution, fewer antral contractions, tonic motor defects, increased outflow resistance in the pylorus or small intestines and impaired distal regulatory mechanisms.[9] Other etiologies for gastroparesis, including idiopathic causes, are less-well understood and may involve inflammatory mechanisms.[10]

However, there is poor correlation between the symptoms of gastroparesis and the severity of delayed gastric emptying. Studies have shown that symptomatic improvement in gastroparesis is only variably correlated with objective improvement in gastric emptying.[11–13] This may be because other pathophysiologic mechanisms (e.g., fundic relaxation, small bowel dysmotility and/or central mechanisms) are improving. However, it is harder to objectively test these factors in clinical practice. It is therfore important to note the distinction between physiologic versus symptomatic improvement of gastroparesis.

Metoclopramide is currently the only medication that is US FDA approved for the treatment of gastroparesis.[14] It was first described by Louis Justin-Besaçon and Charles Laville in 1964 and has been available in the USA since 1979.[15] However, its use has been increasing over the last decade and is estimated by the FDA to be used by over 2 million Americans currently.[16] Given the recent black-box warning issued by the FDA, this review seeks to highlight the clinical efficacy as well as the adverse risks associated with metoclopramide use and to educate healthcare professionals regarding potential ways to mitigate those risks.
 
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Metoclopramide stimulates gut motility by affecting different receptors in the GI tract (Box 1). Most importantly, it acts as an antagonist of the dopamine D2 receptor subtype. Dopamine has a direct relaxant effect on the gut by activating muscular D2 receptors in the lower esophageal sphincter and stomach (fundus and antrum). It also inhibits the release of acetylcholine from intrinsic myenteric cholinergic neurons by activating prejunctional D2 receptors, which leads to an indirect inhibition of the musculature.[29] Metoclopramide promotes gut motility by the following three mechanisms: inhibition of presynaptic and postsynaptic D2 receptors, stimulation of presynaptic excitatory 5-HT4 receptors and antagonism of presynaptic inhibition of muscarinic receptors (Figure 2A). This promotes release of acetylcholine, which in turn leads to increased lower esophageal sphincter (LES) and gastric tone, increased intragastric pressure, improved antroduodenal coordination and accelerated gastric emptying.[30–33] Overall, metoclopramide leads to increased gastric emptying by enhancing antral contractions as well as decreasing postprandial fundus relaxation.[34]However, the prokinetic properties of metoclopramide are limited to the proximal gut.[35]
 
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as my GI attending kept saying.. up to 20% of those who had norovirus.. can develop gastroparesis.. screen for previous cruise ship blues?
 
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I have seen it and as a newly minted CA1 2 weeks in recognized and respected it in a patient undergoing a "quick" EGD/polypectomy (which ended up being 45 min long and difficult). GI doc was pushing for a deep sedation and my attending agreed. I refused and opted for RSI/general c 45 degree inline. Turns out there was ~1000ml residual waiting to be aspirated as she admitted to regurgitating in supine position. GI doc looks over at me, "good call on intubating her, this could have been a mess."

I RSI virtually every patient with gastroparesis and am cautious/leery of diabetics in general when it comes to aspiration risk.
 
I have autoimmune autonomic neuropathy (ganglionoic nicotinic acetylcholine receptor antibody positive) and type 1 diabetes (for 20 years). I also have chronic inflammatory demyelinating polyneuropathy, which can sometimes cause autonomic nervous system damage.

Anyways, I have severe gastroparesis with a gastric neurostimulator (a humanitarian use device) to alleviate my nausea and vomiting.

Here is the answer to your question: This may be TMI but I have vomited up things that are over a day old from my stomach, so yes, these patients are certainly high risk for aspiration. The gastric neurostimulator does not affect gastric emptying time. Premedicating with Reglan likely would be advisable, along with other things. However, Reglan has "side effects" and a lot of gastroparesis patients claim they are "allergic" (Reglan makes me super mean, irritable, and agitated). It can cause tardive dyskenesia so keep this in mind.

Even high blood sugar (180+ mg/dL) can put a person at risk for aspiration, as this delays gastric emptying time, even while fasting, due to build-up of gastric fluids.

FYI: I recently decided to quit pre-med due to medical problems and not going to/not meeting technical standards. I just happened to be browsing the forums.
 
However, there is poor correlation between the symptoms of gastroparesis and the severity of delayed gastric emptying. Studies have shown that symptomatic improvement in gastroparesis is only variably correlated with objective improvement in gastric emptying.[11–13] This may be because other pathophysiologic mechanisms (e.g., fundic relaxation, small bowel dysmotility and/or central mechanisms) are improving. However, it is harder to objectively test these factors in clinical practice. It is therfore important to note the distinction between physiologic versus symptomatic improvement of gastroparesis.

That is very, very true. I have severe gastroparesis, but my symptoms have been very mild in the past, and even now.
 
I have seen it and as a newly minted CA1 2 weeks in recognized and respected it in a patient undergoing a "quick" EGD/polypectomy (which ended up being 45 min long and difficult). GI doc was pushing for a deep sedation and my attending agreed. I refused and opted for RSI/general c 45 degree inline. Turns out there was ~1000ml residual waiting to be aspirated as she admitted to regurgitating in supine position. GI doc looks over at me, "good call on intubating her, this could have been a mess."

I RSI virtually every patient with gastroparesis and am cautious/leery of diabetics in general when it comes to aspiration risk.
This is BS, no offense. The patient should not have been supine, but lateral decubitus, in which case s/he would have not needed intubation. Not only that, but any endoscopist worth her salt will be able to suction a stomach well without the patient risking aspiration. Your attending knows as much endo as I have forgotten. Gastroparesis with a long NPO period (12+ hours), especially in people who had a long bowel prep, is not an indication for intubation for upper endoscopy.

The only case I am intubating such a patient if it's not an elective procedure, or the GERD/achalasia is extremely bad (e.g. they laryngospasm at night) and we are NOT doing an upper endoscopy first. There is more aspiration risk during an airway manipulation with no cough reflexes supine, than during a well performed upper endoscopy with optimal sedation in left lateral position.

Its very laudable that you "RSI" everybody that smells like gastroparesis, but in PP they will chew you up and spit you out if you keep doing this.
 
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We have so many diabetic patients and symptoms dont correlate to risk. We cant RSI every patient. So we just accept the risk that an occasional diabetic patient is going to aspirate?
 
...or maybe we use other screening tools such as diabetes with end organ disease, neuropathy etc.
 
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This is BS, no offense. The patient should not have been supine, but lateral decubitus, in which case s/he would have not needed intubation. Not only that, but any endoscopist worth her salt will be able to suction a stomach well without the patient risking aspiration. Your attending knows as much endo as I have forgotten. Gastroparesis with a long NPO period (12+ hours), especially in people who had a long bowel prep, is not an indication for intubation for upper endoscopy.

The only case I am intubating such a patient if it's not an elective procedure, or the GERD/achalasia is extremely bad (e.g. they laryngospasm at night) and we are NOT doing an upper endoscopy first. There is more aspiration risk during an airway manipulation with no cough reflexes supine, than during a well performed upper endoscopy with optimal sedation in left lateral position.

Its very laudable that you "RSI" everybody that smells like gastroparesis, but in PP they will chew you up and spit you out if you keep doing this.

Your PP comment is fair enough, perhaps I can change my practice when I'm not dealing with a bunch of unskilled clowns in academics. There's only 1 endoscopist I'd let care for my own family at my shop.


If the patient starts coughing when you lower her head below 30-45 degrees because she is regurgitating acid into her pharynx I should ignore her because we have such skilled endoscopists at our academic center? I intubated her in a sitting/45 degree incline because she had severe gerd and I was the only one who recognized it. Its not that I was some stealth CA1, she flat out told me "I can't ever lay flat or I start coughing on acid." Was i supposed to ignore that?


A few other points,

1) I wouldn't have trusted this endoscopist to work on my dog.

2) the scope he initially used was for lasering and he couldn't aspirate much of anything with it so he had to place a second large bore scope to aspirate the contents before he could laser the polyps. Even then, he estimated there was about 250 ml of residual contents that he couldn't aspirate.

3) this wasn't the 10 min procedure he anticipated, it took him at least 45 min before he aborted it because he couldn't laser all of the polyps he had planned to.

4) in the end, all parties involved agreed that an RSI was appropriate.
 
We have so many diabetic patients and symptoms dont correlate to risk. We cant RSI every patient. So we just accept the risk that an occasional diabetic patient is going to aspirate?

There is a simple way of detecting diabetic autonomic neuropathy using a simple EKG test, and I truly hope this helps. Please let me know if this answers your question.

Believe it or not, I actually know the answer to this question, with respect to quickly determining who has diabetic autonomic neuropathy (specifically vagus nerve damage), as a type 1 diabetic patient with autoimmune neuropathies, even though I have no medical training.

The R-R interval can be used as a quick diagnostic "test" for determining vagus nerve damage related to diabetes (diabetic autonomic neuropathy), including both cardiac diabetic autonomic neuropathy and diabetic gastroparesis. I believe the first doctor to find this relationship was an endocrinologist with type 1 diabetes named Richard K. Bernstein.

His article which describes the easy procedure is listed below (an oldie but a goodie):

R K Bernstein
R-R interval studies: a simple office protocol for evaluation of autonomic neuropathy.
Diabetes Care September 1984 7:510-513;

FYI it can be considered effective for determining gastroparesis also (also in type 1s in but this article obviously only type 2s were studied):

Comparison between coefficient of R-R interval variation and gastric emptying in type 2 diabetes mellitus patients.

BACKGROUND:
Autonomic neuropathy is a common complication of diabetes mellitus (DM).

METHOD:
To clarify the relationship between cardiovascular autonomic function and gastric emptying rate, we investigated the gastric emptying and coefficient of R-R interval variation (CV(RR)) of 84 type 2 diabetic patients: 28 cases without peripheral neuropathy and 56 cases with peripheral neuropathy. All patients were subjected to a gastric emptying test according to the marker method (administration of a capsule containing 20 pieces of radiopaque marker during breakfast, followed by abdominal X-ray imaging 3 and 5 h later). Patients had their CV(RR) assessed at rest and during deep breathing.

RESULTS:
Gastric emptying scores were significantly correlated with CV(RR) during deep breathing and with the duration of DM, but neither age nor CV(RR) at rest in all patients. Gastric emptying scores and CV(RR) at rest and during deep breathing in patients with peripheral neuropathy were significantly deteriorated than those in patients without peripheral neuropathy. A significant correlation between gastric emptying and CV(RR) during deep breathing could be observed in the patients with peripheral neuropathy, but not in those without it.

CONCLUSIONS:
These findings showed that CV(RR) during deep breathing might be a good indicator of diabetic gastropathy and that peripheral neuropathy was closely related with cardiac and gastric autonomic neuropathy in the type 2 diabetic patients.
 
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CONCLUSIONS:
These findings showed that CV(RR) during deep breathing might be a good indicator of diabetic gastropathy and that peripheral neuropathy was closely related with cardiac and gastric autonomic neuropathy in the type 2 diabetic patients.
That's well-known. Diabetes produces autonomic neuropathy which translates into gastroparesis and other symptoms, including decreased respiratory variation of the heart rate; one doesn't need an EKG for it, just a pulse oximeter. It's a good idea; maybe I should try it.

The study quoted was done about 3-5 hours after breakfast, while most of our patients are 8-12 hours NPO, which is a different story. We don't know how decreased emptying at 3-5 hours correlates with the risk of aspiration at 8+ hours. Also, no stomach is perfectly empty, even a healthy one, so the question is not only how much stomach content is still there, but also how likely it is to flow back into the esophagus (as in GERD, increased abdominal pressure etc.) which is also difficult to quantify.
 
I can see doing an RSI for patients who have severe GERD in a case where you are already gonna tube, just to avoid positive pressure because I can see that resulting in more frequent aspiration. However for endo, if you rapid sequence every patient with severe reflux, your gonna tune over half of all patients getting scoped! Gastroparesis or not, they should all have been well fasted prior to endoscopy so I see no need. Either way you are gonna see patients with significant residual contents in the stomach because people lie and don't actually fast surprisingly frequently...


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We have so many diabetic patients and symptoms dont correlate to risk. We cant RSI every patient. So we just accept the risk that an occasional diabetic patient is going to aspirate?

Let's get to some real world approaches here:

1. My group has performed in excess of 350,000 anesthetics since I joined them. I have a big "N" to draw from here.
2. We rarely RSI patients who aren't symptomatic (severe gastroparesis or uncontrolled GERD would be RSI) or who don't meet the usual RSI criteria (SBO, Full stomach, etc)
3. 1/2 my group does TIVA for ERCP patients who are jaundiced or at risk (in my opinion). I prefer ETT here.
4. Aspiration is a rare event. But, I have seen it too often(2-5 per year) and it can lead to death or long ICU stays.

Now here is where I disagree with the ASA, some of you and 1/3 of my group. Since I started using PROPHYLAXIS in at risk patients my ASPIRATION RATE is much lower than most of my Group and almost non-existent (only 1 in the past few years and NO ICU STAY was needed). I highly recommend REGLAN AND H2 BLOCKERS to reduce your incidence of aspiration especially clinically significant aspiration. I am aware of ALL THE SIDE EFFECTS of Reglan, Ranitidine, Dexamethasone, etc as I have seen them all. Still, the incidence of peri-operative side-effects is very low when sedation is used prior to the administration of Reglan and selective use of the drug in patient subgroups (avoid in parkisonism, frail/elderly, history of dystonic reactions, crazy women (they get half dose), Psych patients, etc.

The evidence for my statements are ANECDOTAL so feel free to blow me off or ignore me. But, 350,000 anesthetics means I've seen a lot in my career and I'm telling you this stuff works plus it is DIRT CHEAP.

IF you are feeling LUCKY then just place the LMA and hope for the best. But, if you want to tilt the odds in favor of NO MORBIDITY give the Reglan and H2 blocker.
 
I'm sure the "juniors" out there will mouth off about the ETT is the way to go..etc. But, that isn't the way it goes down in many practices. From what I have seen LMAs are used too often in at risk groups WITHOUT prophylaxis which is a setup for aspiration. Sure, the ETT is the way many of you fly on SDN but at the ASC or in many settings the LMA gets used in some "sketchy" circumstances. What I'm preaching here is too increase the odds your OBESE DIABETIC patient goes home or to the floor as planned.

Since aspiration is a rare event I can't prove SQUAT with my prophylaxis treatment except to proclaim that it makes a rare event even rarer.
 
A woman in Connecticut was recently awarded $10.5 million by a jury for a medical malpractice suit against Anesthesia Associates of New London and specifically Drs. Thomas Meitt and Bart Calobrisi (recently deceased) and Jean Richeimer, CRNA. Karla Rosa was a 44 year old patient who went in for surgery in 2006. I'm unable to find the type of surgery she was undergoing. According to the reports, the patient was morbidly obese but she was given a general anesthetic using an LMA.

The patient subsequently aspirated during the operation. She suffered a massive aspiration and was left in a coma for 26 days and stayed in the ICU for nearly a month. She required a tracheostomy and PEG tube for feeding. She also claims memory loss and neurologic, physical, and psychological damages.
 
LMA device for administering anesthesia
A wrongful death lawsuit filed recently in Orange County is not only calling into question the actions of two anesthesiologists, but the constitutionality of the state's civil remedies code as well.

Joann Brown, on behalf of her deceased mother Shirley Brown, filed a lawsuit April 12 against anesthesiologist Dr. Frank Kuang-She Che and nurse anesthetist Michael Ieyoub.

According to the plaintiff's original petition, Shirley Brown, 59, underwent an outpatient gynecological procedure at Memorial Hermann Baptist Hospital in Orange on April 28, 2005.

Che and Ieyoub administered the general anesthesia for the surgery to remove endometrial polyps.

"The surgery itself was uneventful, but at the end of the procedure the patient developed respiratory distress, laryngospasm and hypoxia," the petition states. "Oxygen saturation dropped to as low as 40 percent. A code was called and the patient was intubated with an endotracheal tube and oxygen saturation returned to 100 percent."

Medical records indicate that Brown aspirated stomach contents into her lungs during the procedure and died May 11, 2005, of aspiration pneumonia.

"While under the care and control of the defendants, Shirley Brown continously suffered gross abuse, extensive neglect and undue pain. Mrs. Brown's basic needs were ignored and her dignity was disregarded," the petition states.

The plaintiff alleges that Chen and Ieyoub were negligent because of the way they administered the anesthesia, which was done through a laryngeal mask airway, a device placed into the throat.

In a statement attached to the original petition, Dr. Mark Winik, a board certified anesthesiologist licensed in Maryland and New York, said Brown had several risk factors that should have prompted the anesthesiologists to use a different course of action and administer additional medications.

Winik said Brown's medical records indicate that she was obese, hypertensive and had ischemic heart disease, or a restriction in blood supply to the heart.

Accoring to Winik's statement as an expert for the plaintiff, an obese patient with ischemic heart disease was at an increased risk of aspiration of stomach contents.

"The standard of care … would require the anesthesiologist to administer anesthesia via endotracheal tube as opposed to LMA," Winik stated. "The LMA rests above the vocal cords and provides no protection against aspiration."

The lawsuit also alleges that Chen and Ieyoub were negligent because they failed to administer prophylactic drugs that would have lessened the acidity and volume of gastric secretions in the patient's stomach, such as Alka-Seltzer, Bicitra, Reglan or Pepcid.

"The afformentioned acts and ommissions of defendants constituted negligence per se and such actions were in violation of the legislative statutes passed for protection of the elderly, under the Texas Health and Safety Code," the petition states. The code says that the elderly may not be physically or mentally abused or exploited, must be treated with respect and dignity and may not be denied care based on sex, age or handicap.


"The harm that befell Shirley Brown while under the care of the defendants was the type of harm these statutes were designed to prevent," the plaintiff alleges.

The suit also alleges that the defendants committed a felony by having removed, destroyed or concealed writings.

In addition, "plaintiffs maintain and contend that the Civil Practice and Remedies Code pertaining to medical malpractice is itself unconstitutional" because it limits damage amounts.

The plaintiff says in particular, the limit on recovery of damages based on the number of plaintiffs and violates due process by "creating uneven or disportionate remedies for families because of the number of family members."

Joann Brown is only child of Shirley Brown.

She is seeking damages for medical expenses, mental anguish, impairment, funeral expenses and loss of companionship.

The wrongful death suit also alleges that defendants acted with malice and conscious indifference and therefore the plaintiff is also seeking exemplary and punitive damages.

She is requesting a trial by jury.
 
It makes perfect sense, in selected patients, to decrease stomach acidity and promote emptying. It's a good idea, and the benefits outweigh the risks.
 
Since aspiration is a rare event I can't prove SQUAT with my prophylaxis treatment except to proclaim that it makes a rare event even rarer.

Maybe. I don't do any of the stuff you mentioned and I also see aspiration very, very rarely. The last one I saw was a young healthy patient. Nurse blew way too much air with way too much pressure down an LMA.
 
Lawyers are going to spin things any way they see fit. They are talking about giving Alka-Seltzer for crying out loud!

LMA device for administering anesthesia
A wrongful death lawsuit filed recently in Orange County is not only calling into question the actions of two anesthesiologists, but the constitutionality of the state's civil remedies code as well.

Joann Brown, on behalf of her deceased mother Shirley Brown, filed a lawsuit April 12 against anesthesiologist Dr. Frank Kuang-She Che and nurse anesthetist Michael Ieyoub.

According to the plaintiff's original petition, Shirley Brown, 59, underwent an outpatient gynecological procedure at Memorial Hermann Baptist Hospital in Orange on April 28, 2005.

Che and Ieyoub administered the general anesthesia for the surgery to remove endometrial polyps.

"The surgery itself was uneventful, but at the end of the procedure the patient developed respiratory distress, laryngospasm and hypoxia," the petition states. "Oxygen saturation dropped to as low as 40 percent. A code was called and the patient was intubated with an endotracheal tube and oxygen saturation returned to 100 percent."

Medical records indicate that Brown aspirated stomach contents into her lungs during the procedure and died May 11, 2005, of aspiration pneumonia.

"While under the care and control of the defendants, Shirley Brown continously suffered gross abuse, extensive neglect and undue pain. Mrs. Brown's basic needs were ignored and her dignity was disregarded," the petition states.

The plaintiff alleges that Chen and Ieyoub were negligent because of the way they administered the anesthesia, which was done through a laryngeal mask airway, a device placed into the throat.

In a statement attached to the original petition, Dr. Mark Winik, a board certified anesthesiologist licensed in Maryland and New York, said Brown had several risk factors that should have prompted the anesthesiologists to use a different course of action and administer additional medications.

Winik said Brown's medical records indicate that she was obese, hypertensive and had ischemic heart disease, or a restriction in blood supply to the heart.

Accoring to Winik's statement as an expert for the plaintiff, an obese patient with ischemic heart disease was at an increased risk of aspiration of stomach contents.

"The standard of care … would require the anesthesiologist to administer anesthesia via endotracheal tube as opposed to LMA," Winik stated. "The LMA rests above the vocal cords and provides no protection against aspiration."

The lawsuit also alleges that Chen and Ieyoub were negligent because they failed to administer prophylactic drugs that would have lessened the acidity and volume of gastric secretions in the patient's stomach, such as Alka-Seltzer, Bicitra, Reglan or Pepcid.

"The afformentioned acts and ommissions of defendants constituted negligence per se and such actions were in violation of the legislative statutes passed for protection of the elderly, under the Texas Health and Safety Code," the petition states. The code says that the elderly may not be physically or mentally abused or exploited, must be treated with respect and dignity and may not be denied care based on sex, age or handicap.


"The harm that befell Shirley Brown while under the care of the defendants was the type of harm these statutes were designed to prevent," the plaintiff alleges.

The suit also alleges that the defendants committed a felony by having removed, destroyed or concealed writings.

In addition, "plaintiffs maintain and contend that the Civil Practice and Remedies Code pertaining to medical malpractice is itself unconstitutional" because it limits damage amounts.

The plaintiff says in particular, the limit on recovery of damages based on the number of plaintiffs and violates due process by "creating uneven or disportionate remedies for families because of the number of family members."

Joann Brown is only child of Shirley Brown.

She is seeking damages for medical expenses, mental anguish, impairment, funeral expenses and loss of companionship.

The wrongful death suit also alleges that defendants acted with malice and conscious indifference and therefore the plaintiff is also seeking exemplary and punitive damages.

She is requesting a trial by jury.
 
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PRESENTATION
A 52-year-old man fell from a tree and fractured his ankle. His family brought him to the emergency department of a local hospital at 8:30 p.m. The on-call orthopedic surgeon evaluated the patient and diagnosed a distal comminuted fracture of the left lateral tibia. The patient was scheduled for surgery the next morning. The records indicate that he had a history of coronary artery disease, prior myocardial infarction (MI), hypothyroidism, and depression.

PHYSICIAN ACTION
An anesthesiologist performed a preoperative assessment on the patient the next morning. The patient's son, who was a paramedic, was present. During this interview, the anesthesiologist recommended a spinal anesthetic with endotracheal intubation. The patient's son wanted a general anesthetic in conjunction with a laryngeal mask airway (LMA). The anesthesiologist — who was told that the patient had not eaten since before midnight — agreed to this form of anesthesia. The patient had, in fact, eaten a large meal at 11 p.m. and was taking narcotics for pain.

The surgery was performed without complication until the anesthesiologist removed the LMA and noted that the patient had vomited. The anesthesiologist estimated that less than 1 cc had been aspirated and called for a pulmonology consult and pulmonary treatments.

At 2:14 p.m., eight minutes after arriving in the PACU, the patient vomited coffee ground emesis. A short time later, his oxygen saturations fell from the 70s into the 40s. The respiratory therapist arrived with equipment to intubate and ventilate the patient. The anesthesiologist told her that it was his decision to make and he did not want to intubate the patient. The respiratory therapist later testified that the anesthesiologist "blew her off." At 3:15 p.m., the pulmonologist arrived and recommended that the anesthesiologist intubate the patient immediately. The patient was intubated at 3:17 p.m. and put on a ventilator.

The anesthesiologist recorded that the patient had suffered postoperative hypoxemia secondary to aspiration. The patient's family became very angry with the anesthesiologist and had him removed from the case. The pulmonologist took over the care of the patient, who remained in ICU for 32 days with severe ARDS. The patient was also treated with medication for GERD while in the ICU. He was discharged to a rehabilitation facility. He progressed slowly during rehabilitation because of atrophy of his legs and foot drop.

A neurologist examined the patient and found that he had deficits in short-term memory and impaired speech. The patient was also depressed. An EEG revealed cerebral dysfunction in the left and right frontal temporal areas.

ALLEGATIONS
A lawsuit was filed against the anesthesiologist and allegations included:

  • failure to properly intubate the patient;
  • failure to provide a safe anesthetic technique;
  • failure to institute appropriate measures to prevent aspiration pneumonitis;
  • failure to prevent and treat hypoxemia;
  • failure to timely perform intubation;
  • failure to correctly assess the severity of the patient's acute respiratory failure; and
  • failure to properly document care of the patient and the risks associated with the anesthesia technique.
The patient claimed total disability due to the foot drop and is unable to work.

LEGAL IMPLICATIONS
The defense was unable to locate an expert supportive of the defendant's actions. Overall, the anesthesiologists reviewing this case were critical of the delay in recognizing a significant aspiration event when the patient was in the PACU. When the patient vomited in the PACU, his oxygen saturations decreased for an extended period indicating possible ARDS. The reviewers felt that the anesthesiologist should have immediately intubated the patient and called for a pulmonology consult with bronchoscopy. The respiratory therapist was also very critical of the delay in intubation.

Reviewers were also critical of the decision to use LMA in a patient with a history of GERD and MI. The patient had a 'history that dictated protection of the airway.' However, it is unclear whether or not the family told the anesthesiologist that the patient had been treated for gastric reflux disease and UGI obstruction. Additionally, the anesthesiologist was not informed that the patient consumed a large meal at 11 p.m. while taking narcotics, which can delay gastric emptying.
 
Why do you think the British use the LMA even for laparoscopic surgery? Is it because they just don't give a **** about their patients aspirating, or because there is no relationship between aspiration and LMA use? Association does not mean causation, except for stupid members of the jury.
 
Why do you think the British use the LMA even for laparoscopic surgery? Is it because they just don't give a **** about their patients aspirating, or because there is no relationship between aspiration and LMA use? Association does not mean causation, except for stupid members of the jury.


No Malpractice lawyers means the LMA is safe for Laparoscopic surgery. Plus, they have the published clinical evidence it is a safe approach.

We, on the other hand, are facing a lawsuit EVERY TIME an adverse event occurs in the O.R.
Hence, we don't use LMAs because a million dollars buys a lot of Endotracheal Tubes.
 
Anaesthesia. 2009 Dec;64(12):1289-94. doi: 10.1111/j.1365-2044.2009.06140.x. Epub 2009 Oct 23.
Risk of pulmonary aspiration with laryngeal mask airway and tracheal tube: analysis on 65 712 procedures with positive pressure ventilation.
Bernardini A1, Natalini G.
Author information

Abstract
We compared the risk of pulmonary aspiration in patients whose lungs were mechanically ventilated through a laryngeal mask airway (35 630 procedures) or tracheal tube (30 082 procedures). Three cases of pulmonary aspiration occurred with the laryngeal mask airway and seven with the tracheal tube. There were no deaths related to pulmonary aspiration. The incidence and outcome of pulmonary aspiration detected in this study were similar to those previously reported. The adjusted odds ratio (OR) for pulmonary aspiration with the laryngeal mask airway was 1.06 (95% CI 0.20-5.62). Unplanned surgery (OR 30.5, 95% CI 8.6-108.9) and male sex (OR 8.6, 95% CI 1.1-68) were associated with an increased risk of aspiration and age < 14 years with a reduced risk (OR 0.21, 95% CI 0.07-0.64). There were contraindications and exclusions to the use of the laryngeal mask airway but in this selected population the use of an laryngeal mask airway was not associated with an increased risk of pulmonary aspiration compared with a tracheal tube.
 
We can sit here and debate this age old topic over and over. It always amuzes me when people take a hard and fast line on issues like aspiration or GA vs regional or any other anesthesia topic that has yet to be proven superior. Every pt brings with them some sort of personal bias that we must deal with.

IMO, we all come up with our acceptable risk tolerance. This comes from our training and then from our experiences. The latter carrying more weight. I can't sit here and tell someone on a forum to tube or not tube someone in their Endo suite because I have never been in their endo suite. I don't know the skill level of anyone there. Just like I can't tell anyone on this forum which gastroparesis pt will aspirate. Therefore, arguing about this subject is just arguing to arguing.

I will say this tho. As one of my partners says, " it's just so damn easy to intubate someone so why take unnecessary risks?"
 
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Besides Reglan and co., let's not forget the LMA Supreme. While an OGT does not eliminate the risk of aspiration, it probably decreases the severity significantly.
 
I will say this tho. As one of my partners says, " it's just so damn easy to intubate someone so why take unnecessary risks?"
Yeah, why do we use LMAs at all, except for us being too lazy to put in a tube, especially in obese patients? :whistle:
 
It's sad when I have to put an (obese) patient through the risks and stress of an intubation and intraop ETT, just for the sake of defensive medicine.
 
That was not sarcasm. That was the truth. If you can't handle it, just tell Blade. :p
 
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I will say this tho. As one of my partners says, " it's just so damn easy to intubate someone so why take unnecessary risks?"

Similar to "I've never been sorry I intubated someone, but there have been many times I wish I had."
 
The next time your surgeon requests "MAC OR TIVA" remember this thread. Some of these patients are at increased risk of aspiration and the "cocktail" may prevent a clinically significant aspiration. These are rare events but they still happen; the cocktail makes them even rarer events.
 
Anaesthesia. 1986 May;41(5):486-92.
Premedication with cimetidine and metoclopramide. Effect on the risk factors of acid aspiration.
Pandit SK, Kothary SP, Pandit UA, Mirakhur RK.
Abstract
A randomised, double-blind, placebo-controlled parallel study was conducted in adult females to evaluate the efficacy and safety of a combination of cimetidine 300 mg orally and metoclopramide 10 or 20 mg intravenously in reducing pre-operative residual gastric volume and raising gastric pH. The effect of preoperative metoclopramide on postoperative nausea and vomiting was also investigated. Oral cimetidine was given approximately 2-2.5 hours before, and intravenous metoclopramide either 15 or 30 minutes prior to induction of anaesthesia. The study showed that placebo-treated patients undergoing outpatient operations have an increased risk of acid aspiration because of high residual gastric volume and low pH and increased risk of serious pulmonary injury should acid aspiration occur. Metoclopramide 10 or 20 mg intravenously prior to induction of anaesthesia was effective in reducing the residual gastric volume significantly, but not in raising pH. The combination of cimetidine and metoclopramide, as well as cimetidine alone, reduced the risk factors of acid aspiration by raising gastric pH and reducing residual volume. No anti-emetic effect of metoclopramide was observed. Higher doses of metoclopramide (20 mg) produced significant side effects (flushing, dizziness, extrapyramidal side effects), but were only marginally more effective than 10 mg doses in reducing residual gastric volume.
 
There is no consensus agreement on how to handle Obese patients or Diabetic obese patients who present for surgery (LMA or MAC or TIVA requested by surgeon). Clearly, we aren't going to intubate all of them. Still, Does the "cocktail" help in reducing the incidence and/or severity of aspiration? I say YES. Many others say 'No" and the literature is not convincing in the use of these drugs to reduce aspiration. So why do I use them? Because they MAY help and there is some evidence (weak) that patients avoid serious morbidity with their use. H2 blockers are extremely safe and well tolerated. Reglan is a mixed bag and CAUTION is advised in using it routinely preoperatively without sedation. Instead, I sometimes give 5 mg preop and the other 5 mg with the propofol. Or, I give all 10 mg just prior to the propofol.

For those on the other side of this issue I fully understand your point of view; I just disagree with it. My goal is to DO NO HARM and aspiration,while rare, can be a devastating complication.

Good luck and be careful.
 
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There is no consensus agreement on how to handle Obese patients or Diabetic obese patients who present for surgery (LMA or MAC or TIVA requested by surgeon). Clearly, we aren't going to intubate all of them. Still, Does the "cocktail" help in reducing the incidence and/or severity of aspiration? I say YES. Many others say 'No" and the literature is not convincing in the use of these drugs to reduce aspiration. So why do I use them? Because they MAY help and there is some evidence (weak) that patients avoid serious morbidity with their use. H2 blockers are extremely safe and well tolerated. Reglan is a mixed bag and CAUTION is advised in using it routinely preoperatively without sedation. Instead, I sometimes give 5 mg preop and the other 5 mg with the propofol. Or, I give all 10 mg just prior to the propofol.

For those on the other side of this issue I fully understand your point of view; I just disagree with it. My goal is to DO NO HARM and aspiration,while rare, can be a devastating complication.

Good luck and be careful.

Funny I see this thread today. I've heard about obese and diabetic patients having risks of delayed gastric emptying. Took an NPO 350lb gentlemen back for an ESWL. Ended up tubing the guy as the urologist said we may try to change positioning to prone if we need to get better exposure. And we did.

Anyways, woke the patient up. I pull a lot of folks deep (whole other hot button topic on here I know) but I woke this one up for the simple reason that I hate pulling tubes deep on massive people. Before I pulled the tube, the dude started puking. And puking. And puking. He had to have puked about a liter. Not joking. It was crazy. So yeah, delayed gastric emptying isn't theoretical to me in obese patients anymore.
 
I am "allergic" to Reglan but I did receive an H2 blocker for my gastric neurostimulator surgery (Enterra by Medtronic), before the procedure, when my gastroparesis was absolutely out of control. The neurostimulator alleviated the nausea and vomiting significantly.
 
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