Fioricet

Generic Name: acetaminophen, butalbital, and caffeine (a SEET a MIN oh fen, bue TAL bi tal, and KAF een)
Brand Names: Alagesic, Anolor 300, Dolgic LQ, Dolgic Plus, Esgic, Esgic-Plus, Fioricet, Geone, Margesic, Medigesic, Repan, Zebutal

What is Fioricet?

Fioricet contains a combination of acetaminophen, butalbital, and caffeine. Acetaminophen is a pain reliever and fever reducer.

Butalbital is in a group of drugs called barbiturates. It relaxes muscle contractions involved in a tension headache. Caffeine is a central nervous system stimulant. It relaxes muscle contractions in blood vessels to improve blood flow.

Fioricet is used to treat tension headaches that are caused by muscle contractions.

Fioricet may also be used for purposes not listed in this medication guide.

Important information about Fioricet

Do not use Fioricet if you have used an MAO inhibitor such as furazolidone (Furoxone), isocarboxazid (Marplan), phenelzine (Nardil), rasagiline (Azilect), selegiline (Eldepryl, Emsam, Zelapar), or tranylcypromine (Parnate) in the last 14 days. A dangerous drug interaction could occur, leading to serious side effects.

Tell your doctor if you have ever had alcoholic liver disease (cirrhosis) or if you drink more than 3 alcoholic beverages per day. You may not be able to take medicine that contains acetaminophen. Do not take more Fioricet than is recommended. An overdose of acetaminophen can damage your liver or cause death. Ask a doctor or pharmacist before using any other cold, allergy, pain, or sleep medication. Acetaminophen (sometimes abbreviated as APAP) is contained in many combination medicines. Taking certain products together can cause you to get too much acetaminophen which can lead to a fatal overdose. Check the label to see if a medicine contains acetaminophen or APAP.

Avoid drinking alcohol. It may increase your risk of liver damage while taking Fioricet due to the acetaminophen component.

Before taking Fioricet

Do not use Fioricet if you have used an MAO inhibitor such as furazolidone (Furoxone), isocarboxazid (Marplan), phenelzine (Nardil), rasagiline (Azilect), selegiline (Eldepryl, Emsam, Zelapar), or tranylcypromine (Parnate) in the last 14 days. A dangerous drug interaction could occur, leading to serious side effects. Tell your doctor if you have ever had alcoholic liver disease (cirrhosis) or if you drink more than 3 alcoholic beverages per day. You may not be able to take medicine that contains acetaminophen. You should not take Fioricet if you are allergic to acetaminophen, butalbital, or caffeine, or if you have porphyria.

To make sure you can safely take Fioricet, tell your doctor if you have any of these other conditions:

• kidney disease,
• liver disease; or
• a history of mental illness or suicidal thoughts.

Butalbital may be habit forming and should be used only by the person it was prescribed for. Never share Fioricet with another person, especially someone with a history of drug abuse or addiction. Keep the medication in a place where others cannot get to it.

FDA pregnancy category C. It is not known whether Fioricet will harm an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant while using this medication. Acetaminophen, butalbital, and caffeine can pass into breast milk and may harm a nursing baby. Do not use Fioricet without telling your doctor if you are breast-feeding a baby.

Cocaine Induced Myocardial Infarction

The American Heart Association (AHA) early this month (April 2008) has just came out with a guidelines on the management of cocaine induced myocardial infarction.

Cocaine can cause myocardial ischemia because it blocks the reuptake of norepinephrine and dopamine at the presynaptic adrenergic terminals, thus results in an accumulation of catecholamines at the postsynaptic receptor (powerful sympathetic activities).

The effects of this increased sympathetic activity include:

1. including increased chronotropy and inotropy

2. coronary vasospasm

3. prothrombotic state, and

4. accelerated atherosclerosis — and, in some individuals, can actually cause MI.

But in terms of the symptoms, signs, and diagnostic workup in patients with cocaine-associated MI are similar to those in patients with MI unrelated to cocaine.

However, treatment of cocaine-triggered ischemia and infarct differs in several ways, but the two most important differences are:

1. Benzodiazepines should be given very early; administration of these agents can dramatically reduce and counteract the sympathomimetic effects of cocaine.

2. Beta blockade, because of its unopposed alpha-adrenergic effects, leads to coronary vasoconstriction,increased blood pressure, and increased mortality in cocaine-associated ischemia, and so beta blockers must be avoided in the acute treatment of these patients. 

Other than that, management strategies are almost similar with non-cocaine induced MI (e.g. nitrates and aspirin)

Another point:

In the setting of ST-segment-elevation acute coronary syndromes, primary PCI is better than fibrinolytics because of the relatively high incidence of false-positive ST elevations in patients who have used cocaine.

You can download the AHA guidelines on cocaine induced MI here.

Source: http://emergencymedic.blogspot.com/search/label/myocardial%20infarction

FAST HUG and NICE-SUGAR

FAST HUG is a mnemonic proposed five years ago by Jean-Louis Vincent as a way of assisting healthcare workers looking after critically ill patients. 

The mnemonic stands for: 

F= Feeding 

A = Analgesia 

S = Sedation 

T = Thromboembolic prophylaxis 

H = Head-of-bed elevation 

U = stress Ulcer prophylaxis, and 

G = Glucose/glycemic control. 

All the components are evidence-based and have been used the world over. 

Reference: 

Vincent JL. Give your patient a fast hug (at least) once a day. Crit Care Med. 2005 Jun;33(6):1225-9. 

The above paper requires a subscription for full access and therefore I cannot upload here. 

However, I have found an interesting power point slides that explains rather clearly what FAST HUG is. Click here. 

Further literature search showed that ever since the original FAST HUG has been described by Vincent JL; many other subsequent variants and additions to the original have been proposed and published by many other authors, for example, 

FAST HUG+S (S = Skin care, prevention of pressure ulcer) 

FAST HUG(S) + BID OVER (S = Spontaneous breathing trial; B = bowel care; I= indewelling catheter removal; D= deescalation of antibiotics) 

FAST HUG + EACH HOUR (E = Electrolytes; A = Airway; C = Catheters; H = Hematology; H = Hemodynamics; O = Oral care; U = Urine analysis; R = Relatives) 

FAST HUG + FAITH (F = Fluid balance; A = Aperients; I = Investigation and results; T = Therapies, and Hydration. 

In fact, the variations can go on and on, but to quote the author of the original FAST HUG, Jean-Louis Vincent, who said it succinctly: 

“…….we could continue expanding the mnemonic almost indefinitely, creating long phrases, even poems (!), but this would defeat the original concept underlying the FAST HUG, which was to provide a short and simple mental checklist that can be easily remembered by all staff members, but that includes most important aspects of patient management to be checked whenever attending an intensive care unit patient. A longer mnemonic is less likely to be remembered and hence less likely to be applied” 

Most of original FAST HUG components are relevant to an emergency medicine setting, except for feeding as feeding is usually not started in emergency department ward itself. The “F” for feeding can be substituted to “Fluid resuscitation and management”, which is much more relevant to emergency medicine. 

Specifically for glycemic control, one should read up findings from NICE-SUGAR study, published in NJEM. 

In this multicenter trial, investigators randomized more than 6000 critically ill patients (63% medical; 37% surgical) to either intensive glucose control (target glucose level, 81–108 mg/dL) or conventional glucose control (target glucose level, 144–180 mg/dL). Control of blood glucose was achieved with intravenous insulin infusions. Participants were randomized within 24 hours after admission to intensive care units and were expected to require ICU treatment for 3 or more consecutive days. 

The primary endpoint — death by 90 days after randomization — occurred significantly more often in the intensive-control group than in the conventional-control group (27.5% vs. 24.9%). 

When data were analyzed separately for medical and surgical patients, results were similar to those for the whole cohort. Not surprisingly, severe hypoglycemia (blood glucose level, ≤40 mg/dL) was significantly more common in the intensive-control group than in the conventional-control group (6.8% vs. 0.5%). No differences between the groups were observed in median number of ICU or hospital days or median days of mechanical ventilation or renal replacement therapy. 

This study therefore, suggests that a tight, intensive glucose control could actually harm rather do good to critically ill patients in terms of death and complications of severe hypoglycemia. 

Reference: 

The NICE-SUGAR Study Investigators. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009 Mar 26; 360:1283. 

Note: the full text of this study can be accessed free in NJEM. Click here. 

Source: http://emergencymedic.blogspot.com/search/label/glycemic%20control

Emergency Medicine Digest

1. Prolonged QTc in diabetic ketoacidosis in children

QTc was shown to be prolonged in up to 47% of diabetic ketoacidosis in children and tend to resolves when the ketosis clears (only 13% still with prolonged QTc after recovery).

Implication: Probably monitoring of QT interval in diabetic ketoacidosis in children can be used as a measure of the disease progression?

Reference:

Kuppermann N et al. Prolonged QT interval corrected for heart rate during diabetic ketoacidosis in children. Arch Pediatr Adolesc Med 2008 Jun; 162:544.

2. Nesiritide – Another Disappointing Trial

Nesiritide, a recombinant B-type natriuretic peptide, is approved for as an adjunct for management of acute decompensated heart failure because of its vasodilatory and natriuretic effects.

Previously Follow-Up Serial Infusions Of Nesiritide FUSION I study – shows no benefit from intermittent nesiritide infusions in outpatients with heart failure.

Now, FUSION II study – again shows no benefit of intermittent outpatient nesiritide infusions in high-risk advanced heart failure patients (those in NYHA Class IV, EF 25%). In fact, those with nesiritide has more side effects of hypotension.

Implication:

Initially, when nesiritide was approved for acute heart failure use, I thought that in the future, nesiritide will become a standard drug in all major government (KKM) hospitals and university hospitals. But, well, now that there are more and more disappointing trials, probably this may not become a reality.

Reference:

Yancy CW et al. for the FUSION II Investigators. Safety and efficacy of outpatient nesiritide in patients with advanced heart failure: Results of the Second Follow-Up Serial Infusions of Nesiritide (FUSION II) trial. Circ Heart Fail 2008 May; 1:9.

3. Noninvasive Ventilation (NIV) was shown to be safe and effective as an alternative to immediate endotracheal intubation in acute decompensated heart failure in a retrospective trial.

In fact, the likelihood of in-hospital death was significantly less in the successful-NIV group than in the intubation group. But once the NIV failed (and ultimately required intubation), there is no significant difference in the in-hospital death as compared with those who were intubated earlier.

Implication:

Probably we should put more patients on NIV early (especially those that we anticipate might require respiratory support) but we must be committed to vigilantly and closely observe the patients.

Reference:

Tallman TA et al. Noninvasive ventilation outcomes in 2,430 acute decompensated heart failure patients: An ADHERE registry analysis. Acad Emerg Med 2008 Apr; 15:355.

4. Uninterrupted Manual Chest Compressions During Biphasic Defibrillation?

In this trial, a group of researchers found that that pausing CPR for delivery of shocks might not be necessary because the risk to the rescuer is minimal.

What they did was they measured the leakage voltage and current through mock rescuers while they were still compressing the chests of 43 patients who were receiving external biphasic shocks.

No shocks were perceptible to rescuers (even during delivery of 360 J) and the leakage current measured was found to be below the recommended safety standards.

Implication:

Even though this small trial shows the risk if minimal, I am not sure if anyone of us would be ready to ignore the “one I’m clear, two you’re clear, three everybody clear!” command. One should also remember that the pads used were the pre-gelled electrodes while we were still using the manually applied gel on the electrode pads – when the gel get smeared here and there, I don’t think it is that safe to continue CPR while shock is being delivered.

Reference:

Lloyd MS et al. Hands-on defibrillation: An analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation 2008 May 13; 117:2510.

2010 AHA Guidelines on ECC and CPR

The American Heart Association (AHA) has recently updated the CPR and ECC Guidelines. You can access the full text pdf files of "AHA CPR and ECC Guidelines 2010" articles published in 18 October 2010 issue of Circulation by clickinghere.

The most obvious and sensational change would probably be the change from the A-B-C to the C-A-B sequence of basic life support. In a way, I am not at all surprise of this change given the importance of chest compression ever since the last guidelines published in 2005. Numerous studies in recent years have shown the importance of chest compression, particularly for adult, non-traumatic, sudden onset of cardiac arrest, where the most probable etiology in most such cases would be myocardial infarction and its related arrhythmic sequelae of ventricular fibrillation, ventricular tachycardia, etc etc. In fact, over the last few years, we have seen a tremendous emphasis on chest compression so much so that AHA issued a scientific statement on Hands-Only CPR back in April 2008. At the same time, there is a de-emphasis on ventilation. Too much ventilation has the disadvantage of causing too much interruptions and impediment in our attempts in building up a good coronary perfusion pressure during chest compressions. Too much ventilation causes gastric distention as well, and increases risk of aspiration, reducing effectiveness of chest compression by splinting of diaphragm, In fact, too much ventilation is not necessary as the partial pressure of oxygen in the stagnated blood would have been enough to meet the minimal cellular metabolic demand in a cardiac arrest victim, especially during the first few minutes of arrest.

To me, the five major changes in Guidelines 2010 are:

1. The change from A-B-C sequence to C-A-B

- Beside minimizing delay, the C-A-B sequence also has the advantage over A-B-C because in A-B-C sequence, we are starting CPR with the steps which would be considered most repulsive for the public to initiate CPR (steps A and B). Thus, by using C-A-B sequence, we are encouraging public members to participate in CPR, enabling community empowerment and participation in this vital partnership of resuscitation.

Although no published human or animal evidence demonstrates that starting CPR with 30 compressions rather than 2 ventilations leads to improved outcome, chest compressions provide vital blood flow to the heart and brain, and studies of out-of-hospital adult cardiac arrest showed that survival was higher when bystanders made some attempt rather than no attempt to provide CPR.

2. Look, listen, feel is no longer recommended.

- “Look, listen, and feel for breathing” has been removed from the sequence for assessment of breathing after opening the airway. The healthcare provider briefly checks for breathing when checking responsiveness to detect signs of cardiac arrest. After delivery of 30 compressions, the lone rescuer opens the victim’s airway and delivers 2 breaths.

3. Atropine in cardiac arrest is out

Atropine is not recommended for routine use in the management of PEA/asystole and has been removed from the ACLS Cardiac Arrest Algorithm

4. Adenosine is in.

Adenosine is recommended in the initial diagnosis and treatment of stable, undifferentiated regular, monomorphic WCT

Note: adenosine should not be used for irregular WCTs because it may cause degeneration of the rhythm to VF.

5. Capnograph is in.

Capnography waveform can be used to check whether endotracheal intubation is successful or not, and secondly, it is used to monitor effectiveness of chest compression including achieving ROSC.

Other changes include:

Cricoid pressure

Cricoid pressure applied routinely is out.

Although it can prevent gastric aspiration, cricoid pressure may impede ventilation and interfere with placement of a supraglottic airway or intubation.

If cricoid pressure is used in special circumstances during cardiac arrest, the pressure should be adjusted, relaxed, or released if it impedes ventilation or advanced airway placement.

De-emphasis on pulse check

This guidelines minimizes the importance of pulse checks by healthcare providers. This is because detection of a pulse can be difficult, and even highly trained healthcare providers often incorrectly assess the presence or absence of a pulse when blood pressure is abnormally low or absent. Anyhow, chest compressions delivered to patients subsequently found not to be in cardiac arrest rarely lead to significant injury

Source: http://emergencymedic.blogspot.com/search/label/Advanced%20Cardiac%20Life%20Support

Henoch-Schönlein purpura

Case:

This 7-years old boy was seen in the emergency department about a month ago with the main complaint of sudden onset of colicky abdominal pain. After been given pain relief, his abdomen was soft, non tender and non guarded.He was, otherwise, fully alert and conscious; vital signs are normal, not toxic looking and no signs of meningisms.

The easy part is he has been suspected of having Henoch Schonlein Purpura from his first visit based the skin rash appearance about a week earlier.

However, we should not be misled by any preconceived diagnosis without examining him carefully. If he presented with signs of meningism and appeared toxic looking, the first thing that comes to my mind with that kind of rash appearance would be have been meningococcal septicaemia!! As emergency physician, I must rule out meningococcal septicemia first especially if the history fits. In fact, all literature cited meningococcal septicemia as a differential for the rash per se.

Definition of Henoch-Schönlein purpura (HSP)

HSP is described as non-thrombocytopenic, purpuric and systemic vasculitis of childhood that occurs twice as often in males as in females.

Every word in that definition is keyword to understand HSP:

Henoch-Schönlein purpura is a

Nonthrombocytopenic

- Very important to know that HSP is non-thrombocytopenic because a normal platelet count helps to differentiate HSP from thrombocytopenic purpura

purpuric

- And it is palpable

- Palpable purpura is present in almost 100% of patients with Henoch-Schönlein purpura

- Is a presenting sign in 50% of patients

- Some patients present with predominantly smaller petechial lesions, some present with mainly purpuric lesions, and others present with a mixture of lesion types, some may have target-like lesions (central punctate hemorrhage surrounded by circumferential regions of pallor and hemorrhage)

- The characteristic of the purpura is it is gravity and pressure dependent. This may cause a typical sock line (for those who wear socks regularly – not present in this boy as he did not wear sock)

- Note: The sock line picture is clearly seen in an article by Ponce de Souza et al. in 2005. Click here to go to the article.

systemic vasculitis of

- HSP essentially is an IgA-mediated systemic vasculitis of small blood vessels

- There is diffuse vasculitis secondary to deposition of immune complexes

- Unknown cause but has been associated with various factors, especially a preceding RTI (more than half) particularly a group A strep organism

- Other than that, literature also shows that it has been associated with vaccinations, allergens in foods, drug reactions, etc etc.

- Note: this blog post is not meant to be an exhaustive description of HSP because there are some very good articles available free online. See references below for the links

- Though it is systemic, it is often described as presenting with classical triad of symptoms: a palpable purpuric rash on the lower extremities, abdominal pain or renal involvement, and arthritis.

- This patient has typical rash, as well as severe acute abdominal pain. In fact, when he first arrived in ED, he was groaning in pain, but his pain much improved after given pain relief

- The most serious sequela of HSP is the renal involvement because it can progress to ESRF

- The most common manifestation of renal disease in HSP is hematuria.

childhood

- in fact, HSP is the most common form of vasculitis in children

- Approx 75% of cases occur in children between two and 11 years of age.

- Twice as often in males as in females (this patient is a boy)

References:

Note: these three articles are excellent articles for review.

1. Kraft DM, McKee D, Scott C. Henoch-Schonlein purpura: a review. Am Fam Physician 1998; 58 (2):405-8, 11.

http://www.aafp.org/afp/980800ap/kraft.html

(This article is a good description of HSP, easy to understand)

2. Leung AK, Chan KW. Evaluating the child with purpura. Am Fam Physician 2001; 64 (3):419-28.

http://www.aafp.org/afp/20010801/419.html

(This is a superb article regarding the approach of purpura in general)

3. Ponce de Souza E, Usatine RP. Palpable purpura and a visible sock line. J Fam Pract 2005; 54 (6):520-3.

http://www.jfponline.com/pages.asp?aid=1957&UID=#bib1

(This article has good pictures on the sock lines in the distribution of rash in gravity dependant position. Wonder how the distribution of the rash would be if one of the patient is an astronaut!)

Source: http://emergencymedic.blogspot.com/search/label/acute%20abdomen

Gastrointesntinal Emergencies - A guide for medical students

This notes is not meant to be exhaustive. Look at some of the links below that I have posted. There are excellent articles out there for you to download FOC!

Key Points

History:

A. Relation between abdominal Pain and Vomiting

Generally,

Pain → vomiting = surgical process

Example:

Epigastric pain that is relieved by vomiting suggests intragastric pathology or gastric outlet obstruction

Vomiting → pain = nonsurgical condition

However, this is just a guide, not a rule

B. Pain out of proportion

If patient complained of severe abdominal pain but you find relatively void of physicial findings (“pain out of proportion”) – especially in the elderly, with risk factors like atherosclerotic disease, atrial fibrillation, coronary heart disease, must think of mesenteric ischemia.

C. Duration of pain

Does The Duration Of Abdominal Pain Help In Categorizing Cause?

- Severe abdominal pain that persists for 6 or more hours is likely to be caused by surgically processes.

- Patients with pain of more than 48 hours' duration have a significantly lower incidence of surgical disease than do patients with pain of shorter duration.

D. Pitfalls In Evaluating Elderly Patients With Acute Abdominal Pain

Advanced age - blunt manifestations of acute abdomen

- Pain - less severe

- Fever - less pronounced

- Signs of peritoneal inflammation - diminished or absent

- Elevation of the white blood cell (WBC) count - less sensitive.

Examination

A. Tests For Peritoneal Irritation

Rebound tenderness

Cough test

Heel-drop jarring (Markle) test

- Highly sensitive test for peritoneal irritation

- Patient asked to stand, rise up on tiptoe with knees straight, and forcibly drop down on both heels with an audible thump.

- Among patients with appendicitis, 74% sensitive, compared with 64% for the standard rebound test

o Markle GB: Heel-drop jarring test for appendicitis [letter]. Arch Surg 120:243, 1985.

Obstipation

What is the significance?

Obstipation - the inability to pass either stool or flatus for more than 8 hours despite a perceived need is highly suggestive of intestinal obstruction

Can we give opioids in acute abdomen witb uncertain cause?

- For fear of masking vital symptoms or physical findings, old, conventional surgical wisdom proscribes the use of narcotic analgesics until a firm diagnosis is established.

- Increasingly, however, studies have demonstrated that pain medication may be given to selected patients with stable vital signs because the analgesic effect may be reversed readily at any time by the administration of naloxone.

§ Pace and Burke, in a prospective, double-blind study of 71 patients with acute abdominal pain, found that pain control with morphine had no deleterious effect on preoperative diagnostic accuracy.

- Although inconclusive, a growing body of data suggests that evaluation of acute abdominal disease may be facilitated when severe pain has been controlled and the patient can cooperate more fully.

§ McHale PM, LoVecchio F: Narcotic analgesia in the acute abdomen-A review of prospective trials. Eur J Emerg Med 8:131-136, 2001.

§ Pace S, Burke TF: Intravenous morphine for early pain relief in patients with acute abdominal pain. Acad Emerg Med 3:1086-1092, 1996.

Plain X-ray Films Useful?

Plain films of the abdomen have the highest yield when used in the evaluation of patients with suspected bowel obstruction, intussusception, ileus, and free air secondary to a perforated viscus.

They have much less utility in detecting intraabdominal mass, renal calculi, diverticulitis, gallbladder disease, and abdominal aortic aneurysms

The supine view of the abdomen is the most informative and worthwhile abdominal film. The upright film is superior for visualizing air-fluid levels associated with ileus, obstruction, or biliary air.

The erect chest radiograph is most sensitive for detection of free intraperitoneal air and may show basal pneumonia, ruptured esophagus, elevated hemidiaphragm, air-fluid levels associated with subdiaphragmatic or hepatic abscess, pleural effusion, and pneumothorax.

Air Fluid Pockets

Are air-fluid pocketss within the intestine always abnormal? No

1. The number of pockets:

A study of 300 normal patients by Gammill and Nice shows that although the average number of air-fluid levels was four per patient, some have up to 20 air fluid pockets.

(To remember: if >3, consider might be abnormal (although as said above, it can be up to 20!)

2. The size of pockets

Although typically less than 2.5 cm in length, some were 10 cm.

Easy to remember:

Consider abnormal if (remember 3,6,9):

In Small bowels >3 cm

In Large bowerls >6 cm

In caecum >9cm

Remember the number 3 for small bowels:

>3 cm dilatation

> 3 air pockets

> 3 mm wall thickness

Links:

To know more about Markle test and cough sign: click: http://www.postgradmed.com/pearls.htm

To download a free article on acute intestinal obstruction and acute abdomen (excellent article!!), click:

http://www.fleshandbones.com/readingroom/pdf/233.pdf

To know more about the dilemma in diagnosing causes of acute abdomen in emergency department, click here:

http://www.emedmag.com/html/pre/cov/covers/011502.asp

Two excellent articles in Student BMJ:

1. on acute abdomen, click here:

http://student.bmj.com/issues/00/03/education/56.ph

2. on abdominal radiograph, click here to download a series of articles in pdf:

To download a FREE powerpoint presentation on acute abdomen, click here:

http://www.edu.rcsed.ac.uk/pps/pps83.pps

Source: http://emergencymedic.blogspot.com/search/label/acute%20abdomen