Delirium is one of the most hidden and deadly enemy in ICU. It increases mortality, it cost money and its hard to recognise.
Here is a simple mnemonics for delirium: DELIRIUM(S)
D Drugs, Drugs, Drugs
E Eyes, ears [1]
L Low O2 (MI, ARDS, PE, CHF, COPD) [2]
I Infection
R Retention (of urine or stool), Restraints
I Ictal
U Underhydration/Undernutrition
M Metabolic
(S) Subdural, Sleep deprivation
[1] Poor vision and hearing are considered more risk factors than true causes, but should be "fixed" or improved if possible. Cerumen is common cause of hearing impairment.
[2] "Low O2 states" does NOT necessarily mean hypoxia, rather it is a reminder that patients with a hypoxic insult (e.g. Ml, stroke, PE) may present with mental status changes with or without other typical symptoms/signs of these diagnoses.
An organised effort is underway in the form of website charged by Dr. E.Wesley Ely of Vanderbilt University Medical Center.
http://www.icudelirium.org/
2007年7月28日 星期六
禱告的手...
Prayer Sign (禱告的手) - 評估是否為 difficult intubation.
The prayer sign. The patient is unable to approximate the palmar surfaces of the phalangeal joints despite maximal effort.
Prayer Sign - If patient shows inability to place palms flat together, it suggests difficult intubation. It is a reflection of generalised joint and cartilage immobility and tight waxy skin, particularly in diabetic patients. About 33% of diabetic patients are prone to difficult intubations. One study from Istanbul, Turkey compared 80 diabetic patients (D) with 80 non-diabetic patients (ND) undergoing elective surgery under general anaesthesia. The incidence of difficult laryngoscopy was 18.75% in Group D and 2.5% in Group ND. The incidence of the prayer sign was 31.25% in Group D and 13.75% in Group ND.
Another version of prayer sign is "palm print" method in which grading of the ink impression made by the palm of the hand has been proposed as a means of screening diabetic patients in whom tracheal intubation may prove difficult. In one study, it was found to be superior to 3 other indices - Mallampati classification, thyromental distance and head extension.
References:
The prayer sign. The patient is unable to approximate the palmar surfaces of the phalangeal joints despite maximal effort.
Prayer Sign - If patient shows inability to place palms flat together, it suggests difficult intubation. It is a reflection of generalised joint and cartilage immobility and tight waxy skin, particularly in diabetic patients. About 33% of diabetic patients are prone to difficult intubations. One study from Istanbul, Turkey compared 80 diabetic patients (D) with 80 non-diabetic patients (ND) undergoing elective surgery under general anaesthesia. The incidence of difficult laryngoscopy was 18.75% in Group D and 2.5% in Group ND. The incidence of the prayer sign was 31.25% in Group D and 13.75% in Group ND.
Another version of prayer sign is "palm print" method in which grading of the ink impression made by the palm of the hand has been proposed as a means of screening diabetic patients in whom tracheal intubation may prove difficult. In one study, it was found to be superior to 3 other indices - Mallampati classification, thyromental distance and head extension.
References:
- Relationship of difficult laryngoscopy to long-term non-insulin-dependent diabetes and hand abnormality detected using the ‘prayer sign’ - British Journal of Anaesthesia, 2003, Vol. 91, No. 1 159-1602.
- The palm print as a sensitive predictor of difficult laryngoscopy in diabetics - Acta Anaesthesiol Scand. 1998 Feb;42(2):199-203.
2007年7月25日 星期三
Partial thrombosis 預後較差
NEJM: Partial Thrombosis of the False Lumen in Patients with Acute Type B Aortic Dissection.
In this observational study, researchers examined 201 patients with type B dissection and classified them according to whether the false lumen of the aortic dissection was patent, partially thrombosed, or completely thrombosed. Patients with partial thrombosis of the false lumen, as compared with complete patency, had a significant higher mortality rate at 3 years (31.6±12.4% versus 22.6±22.6%). The partial thrombosis resulted in diastolic and mean arterial blood pressures in the false lumen exceeding the pressures seen in a patent false lumen which may explain these findings.
2007年7月24日 星期二
2007年7月21日 星期六
Osler or Janeway?
如何區分 SBE 病人手上的紅點是 Osler's nodes 或是 Janeway lesions?
Osler's nodes:
Janeway lesions:
- Osler's nodes 會腫痛；Janeway lesions 不會。
- 記法：Osler --> "Ouch" (painful)；node --> "nodular" (swelling).
Osler's nodes:
Janeway lesions:
2007年7月18日 星期三
NEJM: Vit.D 缺乏症
Q: When trying to determine if a patient may have vitamin D deficiency, should you measure serum levels of 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D?
A: 25-hydroxyvitamin D is the barometer for vitamin D status. According to the author of this article, most commercial assays for 25-hydroxyvitamin D are good for detecting vitamin D deficiency. The 1,25-dihydroxyvitamin D assay should never be used for detecting vitamin D deficiency because levels will be normal or even elevated as a result of secondary hyperparathyroidism. The author does warn that because the 25-hydroxyvitamin D assay is costly and may not always be available, providing children and adults with adequate amounts of the vitamin. He believes approximately 800 IU of vitamin D3 per day or its equivalent should guarantee vitamin D sufficiency unless there are mitigating circumstances such as those listed in this table:
Q: What are the causes of vitamin D deficiency?
A: Causes of vitamin D deficiency include reduced skin synthesis (caused by sunscreen use, increased skin pigment, or season and latitude of exposure), malabsorption (Crohn's disease, celiac disease, and bypass surgery), steroids (increased catabolism), breast feeding, liver failure, nephrotic syndrome, and chronic kidney disease. Other causes of vitamin D deficiency include inherited disorders (pseudovitamin D deficiency rickets), primary hyperparathyroidism and granulomatous disorders. See table for complete list.
A: 25-hydroxyvitamin D is the barometer for vitamin D status. According to the author of this article, most commercial assays for 25-hydroxyvitamin D are good for detecting vitamin D deficiency. The 1,25-dihydroxyvitamin D assay should never be used for detecting vitamin D deficiency because levels will be normal or even elevated as a result of secondary hyperparathyroidism. The author does warn that because the 25-hydroxyvitamin D assay is costly and may not always be available, providing children and adults with adequate amounts of the vitamin. He believes approximately 800 IU of vitamin D3 per day or its equivalent should guarantee vitamin D sufficiency unless there are mitigating circumstances such as those listed in this table:
Q: What are the causes of vitamin D deficiency?
A: Causes of vitamin D deficiency include reduced skin synthesis (caused by sunscreen use, increased skin pigment, or season and latitude of exposure), malabsorption (Crohn's disease, celiac disease, and bypass surgery), steroids (increased catabolism), breast feeding, liver failure, nephrotic syndrome, and chronic kidney disease. Other causes of vitamin D deficiency include inherited disorders (pseudovitamin D deficiency rickets), primary hyperparathyroidism and granulomatous disorders. See table for complete list.
Aortic Dissection
86-year-old female presented with syncope.
CXR sign = "calcium sign" of aortic dissection.
Other S/S of aortic dissection:
CXR sign = "calcium sign" of aortic dissection.
Other S/S of aortic dissection:
[Reference]
Young aortic dissection
Question:
Name five physiologic factors (i.e. not genetic disorders) that predispose a patient to a premature weakening of the aortic wall resulting in a greater incidence of aortic dissection at a younger age.
Answer:
1. Bicuspid aortic valve,
2. dilated aortic valve,
3. coarctation of the aorta,
4. pregnancy, and
5. transient profound elevations of blood pressure (e.g. cocaine abuse, weight lifting, Beta-blocker withdrawal)
Reference: Journal of EM, April, 2005, pg. 287
Name five physiologic factors (i.e. not genetic disorders) that predispose a patient to a premature weakening of the aortic wall resulting in a greater incidence of aortic dissection at a younger age.
Answer:
1. Bicuspid aortic valve,
2. dilated aortic valve,
3. coarctation of the aorta,
4. pregnancy, and
5. transient profound elevations of blood pressure (e.g. cocaine abuse, weight lifting, Beta-blocker withdrawal)
Reference: Journal of EM, April, 2005, pg. 287
2007年7月16日 星期一
Submassive PE 不用給 t-PA
Thrombolytic Therapy for Submassive Pulmonary Embolism?
Copyright 2007 by the American College of Emergency Physicians.doi:10.1016/j.annemergmed.2007.01.002
小兒重症何時可用 steroid？
Steroids are indicated in paediatric intensive care as anti-inflammatory drugs or for substitutive treatment. During septic shock, the incidence of adrenal insufficiency (AI) varies between 18 à 52%, depending on the relative or absolute nature of the AI. Contrary to adults, for whom long courses of low doses of corticosteroids were shown to reduce mortality and increased shock reversibility, particularly in those with a negative synacthene test, no study provided sufficient evidence to show a benefit of steroids in terms of outcome in children with septic shock. In neonates, AI occurs frequently after cardiac surgery and the administration of steroids can improve haemodynamic condition. The recommended dose of hydrocortisone during septic shock or after cardiac surgery is 30 to 100 mg/m2/d. Dexamethasone is efficient to reduce postextubation stridor in children and neonate and the rate of reintubations in neonate. During croup, oral or parenteral steroids reduce clinical symptoms. Dexamethasone also reduces the incidence of severe chronic lung disease and the duration of tracheal intubation in premature infants. However the high incidence of side effects, particularly on the central nervous system, makes steroids currently not recommended for bronchopulmonary dysplasia. At last, steroids are indicated for severe asthma and for bacterial meningitis. In this latter indication, dexamethasone was shown to improve neurological outcome, indeed mortality in Haemophilus influenzae and Streptococcus pneumoniae meningitis.
[Reference]
doi:10.1016/j.annfar.2007.03.035
[Reference]
doi:10.1016/j.annfar.2007.03.035
2007年7月11日 星期三
Sepsis 治療進展總整理
Aggressive Sepsis Treatment Lowers Morbidity, Mortality
Back in 2003, after activated protein C received approval for treating severe sepsis and septic shock, I reported on the pathophysiology and treatment of sepsis/SIRS. Since then, there has been much discussion surrounding that important study by Rivers, et al. (N Engl J Med 2001;345[19]:1368.) Simply put, the study demonstrated that septic patients do better if you treat aggressively. This concept has been coined early goal-directed therapy (EGDT).
This study, along with earlier recommendations from the Society of Critical Care Medicine (Crit Care Med 1999;27:723), led to an aggressive approach to septic patients. It has been shown that the first six hours of the patient's treatment has large implications on mortality. (Crit Care Med 2004;32;858.)
Sepsis is defined as a systemic response to infection where there is fever or hypothermia, tachycardia, tachypnea, and evidence of decreased blood flow to internal organs. (Taber's Medical Dictionary. F.A. Davis Company.) Severe sepsis and septic shock are not uncommon, with one study citing an annual average of 282,800 ED visits a year. (Ann Emerg Med 2006;48:326.) Some statistics put it at approximately three percent of all hospital admissions and 10 percent of ICU admissions. (Can Med Assoc J 2005;173[9]:1054.)
Depending on which study one reviews, mortality ranges from 30 percent to 50 percent. The basic pathophysiology concerning sepsis is that SIRS (systemic inflammatory response syndrome) is a host response to either an infectious or non-infectious cause. (Sepsis mimics thyroid storm, toxins/drugs, or neuroleptic malignant syndrome, to name a few.) SIRS includes two or more of the following: temperature greater than 38°C or less than 36°C, heart rate more than 90 bpm (unless on a beta blocker, calcium channel blocker, or a paced rhythm), respiratory rate greater than 20, or leukocyte count greater than 12,000, less than 4,000, or more than 10% bands. Sepsis is defined as two or more SIRS criteria in the presence of a documented or presumed infection. Severe sepsis is further defined as sepsis plus organ dysfunction or hypoperfusion. (Can Med Assoc J 2005;173[9]:1054.)
On a microscopic level, the initial response to the infectious agent is both humoral and cellular with the coagulation and compliment system becoming activated. The endothelium then becomes involved, leading to local ischemia, hypoxia, and increased permeability. This endothelial response is what is thought to lead to the multi-system organ failure often seen in severe sepsis.
Another important concept directly relating to EGDT is oxygen delivery once the above cascade has begun (known as supply-demand mismatch). This is measured by either the Sv02 (using a Swan-Ganz catheter) or Scv02 (using a central venous catheter). Low readings here suggest the cells have to extract a higher percentage of the oxygen delivered, resulting in a lower reading on the venous side. When the supply cannot meet demand, the cells resort to anaerobic metabolism, which results in increased lactate production. Measuring both lactate and Scv02, therefore, are two important components of detecting early sepsis and are crucial in following EGDT.
The most obvious presentation in the septic patient usually relates to blood pressure. Hypotension would be considered by most to be one of the classic criteria of a septic patient. EGDT obviously addresses this by requiring earlier and more aggressive use of vasoactive agents. The protocol suggests 500 ml boluses of either normal saline or colloid up to approximately 2 liters (20-40 ml/kg) with a goal of a central venous pressure of 8-12 mm Hg. A large study compared albumin with normal saline, and found no mortality benefit overall but a trend toward benefit in the sickest patients receiving albumin. (N Engl J Med 2004:350:2247.)
Once the CVP goal is met (in other words, volume resuscitated) and there is continued hypotension, vasopressors are the next step. Mean arterial pressure measurement is what is used in the EGDT protocol, with a target of 65 mm Hg. Although dopamine has been our pressor of choice for years, norepinephrine (Levophed) has had a resurgence recently, partly as a result of a 1998 article showing no end-organ damage in healthy volunteers. (Crit Care Med 1998;26:260.) Therefore, norepinephrine and dopamine are considered first-line agents.
If the patient has persistent hypotension after one pressor, a second is added. Here, one can add either the other first-line agent or epinephrine or vasopressin. Vasopressin has become an agent of interest recently (see current ACLS guidelines), and some advocate its use in sepsis in doses considered physiologic replacement (0.01-0.04 units/min). More about vasopressin will be borne out with the Canadian multicentre Vasopressin and Septic Shock Trial (VASST).
Other recommendations coming out of the Rivers article include early intubation, even with seemingly adequate oxygenation. The thought process behind this is to decrease the work of breathing, to maximize oxygen delivery, and to decrease consumption. Another part of the EGDT protocol is attention to the patient's hematocrit. The recommendation is keeping the hematocrit above 30%, and if below, using PRBC transfusion and inotropic drugs (i.e., dobutamine or milrinone) if the patient is persistently hypotensive after fluids, blood (if necessary), and vasopressors.
Sepsis can cause myocardial depression in approximately 10 percent to 15 percent of patients, and Rivers et al found that adding an inotrope helped raise the MAP. Several other adjunctive therapies which are part of the protocol are tight glycemic control, physiological steroid administration, lung protection while on the ventilator, and the use of activated protein C. In one study, tighter glucose control (80-110 mg/dl vs. 180-200 mg/dl) led to improved morbidity at one year. (N Engl J Med 2001;345:1359.) Low-dose or physiologic-dosed steroids, which have been studied for decades related to sepsis, have been shown to decrease vasopressor requirements (Crit Care Med 1999;27:723) and mortality. (JAMA 2002;288:862.) Lastly, lower tidal volumes (6 ml/kg) also have been shown to decrease mortality. (Circulation 1997;95:1122.) I will discuss activated protein C in next month's column.
Putting all these things together, there are many ways to optimize the patient's outcome.
[Reference]
Isaacs, Lawrence MDEmergency Medicine News:Volume 29(4)April 2007p 3
Back in 2003, after activated protein C received approval for treating severe sepsis and septic shock, I reported on the pathophysiology and treatment of sepsis/SIRS. Since then, there has been much discussion surrounding that important study by Rivers, et al. (N Engl J Med 2001;345[19]:1368.) Simply put, the study demonstrated that septic patients do better if you treat aggressively. This concept has been coined early goal-directed therapy (EGDT).
This study, along with earlier recommendations from the Society of Critical Care Medicine (Crit Care Med 1999;27:723), led to an aggressive approach to septic patients. It has been shown that the first six hours of the patient's treatment has large implications on mortality. (Crit Care Med 2004;32;858.)
Sepsis is defined as a systemic response to infection where there is fever or hypothermia, tachycardia, tachypnea, and evidence of decreased blood flow to internal organs. (Taber's Medical Dictionary. F.A. Davis Company.) Severe sepsis and septic shock are not uncommon, with one study citing an annual average of 282,800 ED visits a year. (Ann Emerg Med 2006;48:326.) Some statistics put it at approximately three percent of all hospital admissions and 10 percent of ICU admissions. (Can Med Assoc J 2005;173[9]:1054.)
Depending on which study one reviews, mortality ranges from 30 percent to 50 percent. The basic pathophysiology concerning sepsis is that SIRS (systemic inflammatory response syndrome) is a host response to either an infectious or non-infectious cause. (Sepsis mimics thyroid storm, toxins/drugs, or neuroleptic malignant syndrome, to name a few.) SIRS includes two or more of the following: temperature greater than 38°C or less than 36°C, heart rate more than 90 bpm (unless on a beta blocker, calcium channel blocker, or a paced rhythm), respiratory rate greater than 20, or leukocyte count greater than 12,000, less than 4,000, or more than 10% bands. Sepsis is defined as two or more SIRS criteria in the presence of a documented or presumed infection. Severe sepsis is further defined as sepsis plus organ dysfunction or hypoperfusion. (Can Med Assoc J 2005;173[9]:1054.)
On a microscopic level, the initial response to the infectious agent is both humoral and cellular with the coagulation and compliment system becoming activated. The endothelium then becomes involved, leading to local ischemia, hypoxia, and increased permeability. This endothelial response is what is thought to lead to the multi-system organ failure often seen in severe sepsis.
Another important concept directly relating to EGDT is oxygen delivery once the above cascade has begun (known as supply-demand mismatch). This is measured by either the Sv02 (using a Swan-Ganz catheter) or Scv02 (using a central venous catheter). Low readings here suggest the cells have to extract a higher percentage of the oxygen delivered, resulting in a lower reading on the venous side. When the supply cannot meet demand, the cells resort to anaerobic metabolism, which results in increased lactate production. Measuring both lactate and Scv02, therefore, are two important components of detecting early sepsis and are crucial in following EGDT.
The most obvious presentation in the septic patient usually relates to blood pressure. Hypotension would be considered by most to be one of the classic criteria of a septic patient. EGDT obviously addresses this by requiring earlier and more aggressive use of vasoactive agents. The protocol suggests 500 ml boluses of either normal saline or colloid up to approximately 2 liters (20-40 ml/kg) with a goal of a central venous pressure of 8-12 mm Hg. A large study compared albumin with normal saline, and found no mortality benefit overall but a trend toward benefit in the sickest patients receiving albumin. (N Engl J Med 2004:350:2247.)
Once the CVP goal is met (in other words, volume resuscitated) and there is continued hypotension, vasopressors are the next step. Mean arterial pressure measurement is what is used in the EGDT protocol, with a target of 65 mm Hg. Although dopamine has been our pressor of choice for years, norepinephrine (Levophed) has had a resurgence recently, partly as a result of a 1998 article showing no end-organ damage in healthy volunteers. (Crit Care Med 1998;26:260.) Therefore, norepinephrine and dopamine are considered first-line agents.
If the patient has persistent hypotension after one pressor, a second is added. Here, one can add either the other first-line agent or epinephrine or vasopressin. Vasopressin has become an agent of interest recently (see current ACLS guidelines), and some advocate its use in sepsis in doses considered physiologic replacement (0.01-0.04 units/min). More about vasopressin will be borne out with the Canadian multicentre Vasopressin and Septic Shock Trial (VASST).
Other recommendations coming out of the Rivers article include early intubation, even with seemingly adequate oxygenation. The thought process behind this is to decrease the work of breathing, to maximize oxygen delivery, and to decrease consumption. Another part of the EGDT protocol is attention to the patient's hematocrit. The recommendation is keeping the hematocrit above 30%, and if below, using PRBC transfusion and inotropic drugs (i.e., dobutamine or milrinone) if the patient is persistently hypotensive after fluids, blood (if necessary), and vasopressors.
Sepsis can cause myocardial depression in approximately 10 percent to 15 percent of patients, and Rivers et al found that adding an inotrope helped raise the MAP. Several other adjunctive therapies which are part of the protocol are tight glycemic control, physiological steroid administration, lung protection while on the ventilator, and the use of activated protein C. In one study, tighter glucose control (80-110 mg/dl vs. 180-200 mg/dl) led to improved morbidity at one year. (N Engl J Med 2001;345:1359.) Low-dose or physiologic-dosed steroids, which have been studied for decades related to sepsis, have been shown to decrease vasopressor requirements (Crit Care Med 1999;27:723) and mortality. (JAMA 2002;288:862.) Lastly, lower tidal volumes (6 ml/kg) also have been shown to decrease mortality. (Circulation 1997;95:1122.) I will discuss activated protein C in next month's column.
Putting all these things together, there are many ways to optimize the patient's outcome.
[Reference]
Isaacs, Lawrence MDEmergency Medicine News:Volume 29(4)April 2007p 3
STOP sepsis bundle
為了讓我們 AICU 的敗血症重症患者可以得到更完善、一致的照顧，我們引進了 STOP Sepsis(Strategy to Timely Obviate the Progression of Sepsis) Bundle，做為 sepsis 重症患者的診療依據及 ICU 的品管指標之一。
新光吳火獅紀念醫院急診醫學科 印制
Lecture slides:
2007年7月5日 星期四
May-Thurner Syndrome
- The May-Thurner syndrome is the symptomatic compression of the left common iliac vein between the right common iliac artery and the lumbar vertebrae.
- In 1851, Virchow observed the sinistral (left-sided) predominance of deep venous thrombosis of the legs and proposed this explanation.
- More than a century later, May and Thurner noted the presence of venous webs, or “spurs,” in the left common iliac vein in 22% of autopsies. They attributed these spurs to scarring from repetitive compression of the common iliac vein by pulsations of the overlying common iliac artery.
- Compression of the iliac vein has been documented in approximately 50% of patients with left iliac vein thrombosis.
http://content.nejm.org/cgi/reprint/357/1/53.pdf
Thromboembolism
Pulm. embolism
- Q: Does a normal level of oxygen saturation on pulse oximetry rule out pulmonary embolism?
- A: A normal level of oxygen saturation on pulse oximetry does not rule out pulmonary embolism. However, a rapid pulse is a nonspecific finding that is often, but not always, seen in the presence of thromboembolism.
- Q: Does oral contraceptive use increase the risk for deep venous thrombosis? Does it make a difference how long the woman has been using oral contraceptives?
- A: Oral contraceptives increase the risk for deep venous thrombosis. Depending on the preparation, oral contraceptives can increase the risk of DVTs by a factor of two to five. The greatest risk occurs during the first 6 months of use.
2007年7月3日 星期二
Diagnosis at a glance
一位 2 個月大 baby 因 seizure 就醫，檢查發現 hypocalcemia。
Chest x-ray 如下，請問診斷是？
Hint: 請對照看以下另一位正常小 baby 的 CXR：
答案應該知道了吧？
對，就是 DiGeorge Syndrome。 請仔細看病人的 CXR：mediastinum 是窄的，因為少了 thymus！The DiGeorge syndrome is an example of a selective T-cell deficiency caused by the failure of development of the third and fourth pharyngeal pouches.
These pouches give rise to the following structures:
[Reference]
Radiology Cases in Pediatric Emergency Medicine
Loren G. Yamamoto, MD, MPH
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
Chest x-ray 如下，請問診斷是？
Hint: 請對照看以下另一位正常小 baby 的 CXR：
答案應該知道了吧？
對，就是 DiGeorge Syndrome。 請仔細看病人的 CXR：mediastinum 是窄的，因為少了 thymus！The DiGeorge syndrome is an example of a selective T-cell deficiency caused by the failure of development of the third and fourth pharyngeal pouches.
These pouches give rise to the following structures:
- thymus
- parathyroid
- saortic arch
- portions of the lips and ears
[Reference]
Radiology Cases in Pediatric Emergency Medicine
Loren G. Yamamoto, MD, MPH
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
2007年7月2日 星期一
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