Muhammad Aamir Latif High Yield Notes
1. Troponin enzyme: Write Tro-po-nin-6 and now remember Troponin 6. see how many letter are in word troponin? 8 so
now write Troponin 6 & 8. Troponin level arises 6 hours after AMI and remains elevated for about 6+8=14 days.
CK-MD: how many letters 4, so follow the rule of 4.It starts 4 hours after AMI and remain elevated uptil 4 days.
Myoglobin: write Myo…..Globin. I split the word Myoglobin into 2 so it arises 2 hours after AMI. This is the earliest
enzyme level to be detected. Which one is more specific? Troponin.
2. Systolic BP <90, HR <60 or >100, and RV infarction or who have taken any phosphodiesterase inhibitor for erectile
dysfunction within the last 24 hours (extend timeframe to 48 h for tadalafil).are a contraindications to nitrate use in MI.
3. The optimal approach is to administer thrombolytics as soon as possible after onset of symptoms (up to 12 h from
symptom onset according to some authors) in patients with ST-segment elevation greater than 1 mm in 2 or more
anatomically contiguous ECG leads, new or presumed new left bundle-branch block, or anterior ST depression where
posterior infarction is suspected. With ST-segment elevation, the diagnosis is relatively secured; therefore, initiation of
reperfusion therapy should not be delayed for the results of cardiac markers.
4. Administer a platelet glycoprotein (GP) IIb/IIIa-receptor antagonist (eptifibatide, tirofiban, or abciximab), in addition to
aspirin and unfractionated heparin, to patients with continuing ischemia or with other high-risk features and to patients
in whom PCI is planned. Studies suggest that the addition of intravenous platelet glycoprotein (GP) IIb/IIIa-receptor
antagonists to aspirin and heparin improves both early and late outcomes, including mortality, Q-wave MI, need for
revascularization procedures, and length of hospital stay. MI.with st elevation. pain less then 12 hr and with in 30 min
of showing in ER BUT st elevation in more then 2 leaads.TPA with in 90 min of showing in ER angioplasty
mortality is reduced by angioplasty so it is prefered to angioplasty within 90 min
5. In patients treated with fibrinolytic therapy, recommendations for heparin therapy depend on the fibrinolytic agent.
Heparin has an established role as an adjunctive agent in patients receiving alteplase, reteplase, or tenecteplase but
should not be used with nonselective fibrinolytic agents such as streptokinase and anistreplase.
6. An ACE inhibitor (Captopril) should be given orally within the first 24 hours of STEMI to patients with anterior
infarction, pulmonary congestion, or left ventricular ejection fraction (LVEF) less than 40% in the absence of
7. Beta-blockers are beneficial in patients with atherosclerotic coronary lesions and, when used in conjunction with other
drugs (calcium channel blockers and nitrates), they are useful to achieve control of symptoms. Nevertheless,
nonselective beta-blockers can potentially have detrimental effects in some patients with CAS due to their effect on
beta-2 receptors that physiologically mediate vasodilatation. Thus, when used in patients with CAS, beta-blockers may
induce coronary spasm worsening vasospastic angina. Beta-blockade may also place the patient at risk for unopposed
alpha activity in the setting of cocaine-induced vasospasm. If life-threatening arrhythmias are documented, defibrillator
implantation may be considered for secondary prevention because the risk for sudden cardiac death is about 2%.
Coronary angioplasty may be indicated in rare cases of medically intractable CAS. Stent implantation may successfully
serve as a scaffold to maintain patency in spastic areas that are refractory to medical therapy. The efficacy of coronary
bypass is greater in patients with associated coronary atherosclerotic lesions.
8. During inspiration Right sided murmuer Increases due to increase venous return. During expiration left sided murmur
9. 16 year old boy came for routine physical. BP120/80, Pulse 72, S2 widely split. Doesn‘t change with respiration. Grade
2/6 Mid systolic murmur heard on pulmonary area. A middiastolic murmur best heard over left sternal border. Dx?
10. Intraaortic ballon counterpulsation decreases afterload.
11. Pt. with shortness of breath JVP increased, hypotensive, has paradoxical pulse of 20 mmHg. In EKG amplitude
changes with each heart beat. Most likely Dx? Temponade. Electrical alternate with each heart beat.
12. 22 year old female in 3rd
trimester came for routine physical has grade I systolic murmur on left sternal border which
disappear on standing and valselva. Dx? Functional murmur Cx? Due to increased CO in late pregnancy.
13. Pt. with mechanical valve has INR of 2. What to do next? Increase the dose of coumadin to maintain INR to 2.5 to 3.5.
because we normally keep the INR b/w 2 to 3.
14. PDA connects the descending aorta and pulmonary artery. In maternal rubella infection early pregnancy can cause
PDA. Dx in premature. Which drug can help close the PDA? Indomethacin. TOF: MC Cyanotic congnital cardiac
anomaly. Child while playing become very short of breath and cyanotic and even passes out and turns blue while
playing. Dx TOF. TOGA. From left vertricle pulmonary artery comes out. RV aorta is attached. They will be cyanotic
from birth. Need urgent surgery.
15. COA. Young female with COA think about turner syndrome.XO. Pt has HTN, femoral pulses low, systolic murmur on
the back. CXR notching of rib. Scalloping of the ribs. Dx? COA.
16. We do Synchronised cardioversion except in ventricular fibrilations or pulseless V tachycardia.
17. 73 year old pt h/o CAD with symptoms occasional palpataions, while in the emergency room on cardiac monitor Pt
develop Asystole what to do next? Always check in the 2nd
lead when patient develop asystole. Next? Transcutaneous
Pacemaker placement followed by transvenous pacemaker. Also can give atropine & epinephrine alternatively.
18. Pt comes with A. fib first rule out thyrotoxicosis.
19. Pt come with BP 230/130, c/o chest pain which of the following antihypertensive would be appropriate to you? IV
nitroglycerine. Pt. started on IV Nitroglycerine c/o headache, what to do next? Tell the pt it is a very common side
effect. If it is intolerable then you can have to discontinue otherwise continue. Pt. on nitroglycerin started turning blue.
Pulse oximetry 98%, most likely Dx? Methemoglobinemia. What to do next? Discontinue IV nitrate and give patient
20. Pt. with BP >230/130 started on IV nitroprusside nurse forget to use the pump. Pt become confused develops seizure
Dx? Cyanide toxicity. Tx? Stop the drug and give amylnitrite (it will create methemoblobinemia which will bind with
free cyanide ions.
21. What is the most imp factor in life style change for hypertensive patient? Weight reduction. CAD most important life
style modification is? Stop smoking.
22. 80 year old male 180/80 on Amlodipine. Which of the following drug would you like to add? Diuretic (Isolated systolic
HTN). 60 year old h/o Asthma, 150/90 BP besides advising life style modification. Which of the following drugs
would you like to add? Diuretic or beta blockers (CI in ashma). Pt with symptoms of angina + HTN. DOC? Beta
blockers. DM + HTN. DOC? ACEI
23. H/o HTN started on ACEI c/o cough (dry) what to do next. Discontinue ACEI. What can we use? ARB (receptor
blocker. 60 year old h/o HTN started on Ca channel blocker C/o leg swelling, denies exertional shortness of breath. O/E
lungs are clear. Anckle edema present. What to do? Discontinue CCB. Pt with HTN on Verapamil c/o constipation?
24. Cardiomyopathy treatment: Dilated (ACE, ARB, Beta blocker, Spironolactone) Hypertrophic (Beta blocker, Diuretics),
Restrictive (Diuretics and treating the underlying cause).
25. HTN + CHF again drug of choice? ACEI. HTN + Gout? Avoid Diuretics. HTN + BPH? DOC Alpha blocker.
26. HTN + having serum Na 150, K 2.8 Dx? Primary hyperaldosteronism. Next? Renin/ Aldosterone level. Next? CT abd.
When you have choice of renin, aldosterone, and CT abd. Pick up CD abd b/c only ratio can help and aldosterone alone
not. CT Abd will tell us whether it‘s Adrenal Adenoma (MC) or Bilateral Hyperplasia. If patient has Adenoma (I think
size will be more tha 4, have to confirm) then go for surgery and if it‘s bilateral adrenal hyperplasia then DOC is
Spironolactone (Aldosterone antagonist).
27. HTN pt. h/o recurrent palpataion, headache, diaphoresis, anxiety. O/E postural hypotension. What investigation would
you like to do? 24 hours urine metanephrine or catecholamine. Now we prefer metanephrine rathar than VMA as
former is more sensitive. Next step? CT abdomen. Prior to surgery give Alpha blocker Phenoxybenzamine.
28. DOC for HTN in pregnancy? Methyldopa or hydralazine or labetalol or B Blocker (can cause fetal growth retardation).
Avoid B blocker in prinzmetal angina but we normally give beta blocker in other angina patients.
29. Acute Coronary syndrome we can‘t differentiate unstable angina and acute NSTMI. Order Cardiac enzymes.
30. When ACEI in MI? if pt is not hypotensive within first 24 hours unless serum creatinine is 2.5 and can be continue if pt
has low ejection fraction or CHF.
31. CCB if pt was on short acting Dihydropyridine like Nifidipine should be discontinued why? b/c they can cause reflex
tachycardia but you may continue if pt was on non-dihydropyridine. Dihydropyridine Does cause reflex tachycardia
while non no cause tachycardia.
32. Check Cholesterol level and statin should be started on all MI patients prior to hospital discharge.
33. Aldosterone antagonist spironolactone or eplerenone (Less S/E) recommended for post MI pt. with LV dysfunction or
34. Pt. came to ER have MI which of the following medication should discontinue which patient was already on? CCB
35. CP + SOB what should we do? Check vital and do ABG? If pt on O2 inhalation and desaturated. What should we do?
Intbate the patient.
36. Kussmaul‘s Sign: Normally JVP decreases on inspiration. But when it increases on inspiration it is called kussmaul
37. While waiting to go to CCU, MI pt in ER develop bradycardia what to do? Use Atropine, bradycardia. What to do? Use
atropine if doesn‘t improve use transcutaneous pacemaker.
38. Pt. Develop A fib use IV B blocker. Metoprolol or IV CCB. If vitals unstable go for cardioversion.
39. Pt. Develop non sustain V tachycadria (which last less than 30 sec. what to do? Observe these patients. If recurrent non
sustain V tachy cardia then what to do? Increase the dose of B blocker or start Amiodarone. V tachy cardia, Vitals
stable (Use amiodarone), vitals Unstable (Cardioversion) we can use Lidocaine but prefered amiodarone. V Fib what to
do? Start CPR and use defibrilation (two typee: Monophasic 360J, Biphasic 200J) if doesn‘t get better use epinephrine
or vasopression or another shock. Still not get better Amiodarone then another shock. Check K and Mg level in this pt.
Patient has premature ventricular beats. What to do? No treatment so nothing to worried about. Pt. develops asystole.
Again check in 2nd
lead if you confirm in another lead then? Tx is transcutaneous pacemaker then you can use
Epinephrine, Atropine alternatively.
40. Most Common Cause of Asystole is Hypoxia and electrolyte imbalance.
41. Pt. Develop 1st
degree AV block. What to do? Nothing to worry about. 2nd
degree AV block Mobitz Type I
Asymptomatic no treatment. Mobitz type II Pacemaker. 3rd
degree get pacemaker. First give transcutaneous pacemaker
and then get transvenous pacemaker.
42. While treating MI Pt was giving NTG, BB, morphine, ACEI. Pt became hypotensive. What to do next? Give NS and
examine the pt. If you have given the thrombolytic and if heart sounds are distant then check EKG. If EKG show low
voltage check Echocardiogram to check or rule out Hemorrhagic pericarditis. If NS is not effective you can use
vasopression. Still in shock? Intraaortic ballon counterpulsation.
43. MI pt admitted in CCU. After 5 days c/o sudden onset of shortness of breath. Bilateral crackle present, new systolic
murmur radiating to axilla. Dx? Acute MR sec to rupture chordie tendene 2 to 7 days after MI. Tx? Surgery. Same
history as above systolic murmur at left lower sternal border. Swans Gang Catheter shows increased O2 saturation from
Rt. Atrium to Rt. Ventricle Dx? VSD. Post MI pt has persistant ST segment elevation even after 4 to 8 weeks Dx?
Aneurysm of left ventricle. Post MI after 4 days c/o CP, worse with inspiration and supine. Relieve by sitting Dx?
Pericarditis next? Prescribe Aspirin or indomethacin. How would you confirm? ECHO. Four week after MI, pt comes
to ER c/o fever, CP; Characteristics of pericarditis, Routine labs shows increased WBC. Dx? Dressler syndrome.
Autoimmune problem usually occur after 1 to 12 weeks after MI. Tx? Give aspirin or indomethacin if don‘t get better
then give Steroids.
44. Post MI pt plan for discharge. Echo sugggest EF < 40% which of the following medications will be useful to this pt?
45. Post MI patient want to resume sexual aactivity? 2 to 4 weeks.
46. 35 year old smoker c/o CP has ST depression. T wave inversion Cardiac enzyme –ve, started on NTG, heparin, Aspirin,
BB, After 24 hours he doesn‘t have any CP. Cardiac enzyme are –ve. EKG still has ST depression and T wave
inversion? What to do? Send him for Cardiac Catherization.
47. 60 year old Substernal CP while sowelling snow pain relieved with sublingual NTG, EKG is normal. What to do?
Admit the pt for possible unstable Angina. DM pt with angina on nitrate, aspirin still c/o exertional CP. What to do?
Add BB. Young Pt. with CP has no risk factors suspect Cocaine abuse. Young male cocaine abuser. EKG may have ST
elevation due to vasospasm. Rule out MI. Which of the following should be avoided in cocaine abuser? Thrombolytic
Why? Because it is vasospasm that is causing MI and not blood clot.
48. Hypothermic pt has V.Fib or Cardiac arrest unresponsive to resusitation. Continue CPR until pt has been rewarmed at
least 32C preferably >35C. In severe hypothermic internal rewarming is more important than external. Extracorporeal
blood rewarming prognosis in hypothermia is poor if pt has severe metabolic acidosis <6.6.
49. IV drug abuser came with fever, cough, hemoptysis, CP, CXR shows multiple nodular densities. Was diagnosed with
endocarditis, started on Vanco+Genta. After 7 days pt is still febrile, repeat blood culture was drawn which show Staph
Aeurus resisting to methicillin but sensitive to Vancomycin. What to do? Call surgical consult coz pt have persistant
fever. Pt. on treatment endocarditis develops complete heart block? Dx? Myocardial abscess. To confirm you have to
do TEE, Next step? Call surgical consult. Endocarditis pt with blood culture developing clostridium septicum or
streptococcus bovis, besides treating this infection. What will be the next evaluation? Colonoscopy.
50. End stage renal pt on hemodialysis via dialysis catheter came with c/o fever chill. O/E Exit site of catheter has some
erythema and tenderness. There is no tenderness on tunnel. What to do after sending the blood culture? Choice will be
1- remove the catheter + Give Vanco+ Genta, 2-Give Vanco + Genta. When you have only erythema and tenderness
just at the exit site you don‘t need to remove the tunnel. We remove the catheter when pt is in septic shock
(Hypotension, tachycardia, diaphoretic, running high fever ) or if there is tenderness on the tunnel on pressing the
tunnel, discharge coming out in those situation you have to remove the catheter.
51. H/o exertional SOB comes with worsenig SOB. Also complains of paryxysmal nocturnal dyspnea, cough. O/E Bilateral
Diffuse crackles presents. Lower extremities edema may or may not be present. JVP may or may not be elevated. CXR
has bilateral congestion cardiomegally Dx? CHF always rule out MI. Investigation of choice is Echo, Can tell systolic
dysfunction or diastolic dysfunction.
52. ACEI decrease afterload. Use Digitalis only in systolic dysfunctions.
53. What is the difference b/w systolic and diastolic dysfunction.managment? You first decrase the heart rate of the patient.
54. Which of the following drugs decrease hypertrophy of the heart? Angiotensin Type II receptor blockers are the best.
55. Pt SOB has exersional swelling of the legs what to do? Check ABG.
56. Volume overloads CHF. It may be nephrotic syndrome so also check UA. Both get better with Diuretics.
57. In acutely decompensated heart we don‘t Use BB. When can you use BB? Just before pt is being discharged or when pt
come for the follow up or when you have confirm diastolic functions on ECHO than you can use BB.
58. Hyperkalemia. Fist drug to use? Calcium but when there is digitalis toxicity don‘t use calcium.
59. 50 year old Male c/o passing out, work up suggests restrictive cardiomyopathy. UA suggest proteinuria. H/o easy
bruising constipation and dirrhoea, recently diagnosed carpel tunnel syndrome. Most likely Dx? Amyloidosis.
60. We don‘t tap the pericardial effusion b/c they get resolved by itself. But for cardiac tamponade we use TAP.
61. 30 year old female c/o progressive edema, recently, started feeling dull RUQ pain, weakness, easy fatiquability.O/E
lungs are clear edema leg, JVP increased, hepatojugular reflex present. EKG shows right ventricular Hypertrophy.Dx?
Primary Pulmonary hypertension.Young female with sign of RHF suspect primary pulmonary HTN. Which
investigation? ECHO. Tx? No specific treatment all the drugs are in trial. You can give CCB may help, Doing trial with
62. Pt with elevated JVP, on inspiration JVP increases (Normally during inspiration. JVP decreases) Called + Kussmail
sign. Found in Right Ventricular infarct, Constrictive pericarditis. H/o Cancer of breast Status post radiation therapy
came with c/o SOB, CP could have constrictive pericarditis or pericardial effusion. Pt. coming from Southeast Asia c/o
fever night sweat could have TB pericarditis. Differentiate Constrictive pericarditis ( SOB, Inc JVP, Kssmail sign +ve,
Heart size Normal, h/o TB or radiation ) Pericardial Effusion ( SOB Inc JVP, Pulsus Pericarditis, Heart size increased,
low voltage EKG electrical alternan ). In constrictive pericarditis first use Diuretic and if still symptomatic then
surgically remove pericardium.
63. Pt. CA breast c/o SOB. O/E has feeble heart sound, accentuated fall in BP (systole during inspiration Dx? Tamponade.
64. 40 year old male c/o SOB on exertion, history suggest heavy smoker, alcohol abuse. O/E Basal crackles present. CXR
cardiomegally. EKG sinus Tachycardia. ECHO LV dilated Cardiac cath shows coronaries are normal. Dx? Dilated
Cardiomyopathy. Due to Alcohol abuse. Advice? Stop alcohol. Same sumptoms as above instead of alcohol pt may be
portpartum or taking chemotherapy Adriamycin. In these situations they can develop dilated cardiomyopathy.
65. 20 year old while playing football passed out for 2 minute, O/E has sustained apical impulse, systolic murmur, which
increases with Valselva and standing Dx? HOCM, investigation? ECHO. Tx? BB or dual chamber pacemaker (have
found to decrease hypertrophy). Pt has malignant ventricular arrythmias or past family h/o sudden death. In these two
situation use Implantable defibrillator. Pt on Dx of HOCM shouldn‘t participate in competitive sport. Young patient
with h/o syncope while playing football. Exam doesn‘t show HOCM. EKG shown on exam Dx? Long QT syndrome.
In Long QT syndrome also has h/o deafness. How do you Mx? Same as HOCM. MCC of A fib? HTN.
66. PE gives fever why? Due to clot. Pneumothorax gives fever why? Atelectasis. Blood collection also gives fever. MI
give fever because I‘ts also a clot.
67. What is your maximum heart according to your age? 220 – your age.
68. More blood more murmur except IHHS n MVP and all are treated with Preload reduction with Diuretics, When IHHS
and MVP are treated with Diuretics? Never.
69. VT in stable pt? Tx Lidocaine, VT in unstable pt? Tx? Shock
70. Doses to be remember for ACLS. Epinephrine 1 mg, Atropine 1mg, lidocaine 1mg/kg.
71. Asystole: In medicine, asystole (colloquially known as flatline) is a state of no cardiac electrical activity; hence no
contractions of the myocardium and no cardiac output or blood flow. Asystole is one of the conditions required for a
medical practitioner to certify death When a patient displays asystole, the treatment of choice is an injection
of epinephrine and atropine (vasopressin may also be used) 
and chest compressions. In asystole, the heart will
generally not respond to defibrillation because it is already depolarized. However, some emergency physicians
advocate a trial of defibrillation in case the rhythm is actually fine ventricular fibrillation otherwise indistinguishable
from asystole, although little evidence exists to support the practice. Asystole is usually a confirmation of death as
opposed to a heart rhythm to be treated, although a small minority of patients is successfully resuscitated if the
underlying cause is identified and treated immediately. Generally, after a minute and a half to five or so minutes, the
heart will not respond to defibrillation or injections of epinephrine and atropine (if ventricular fibrillation or asystole is
still present) and the patient is then declared dead or brain-dead. The victim will then be put on cardiopulmonary
bypass and dialysis if his heart, lungs, liver, and kidneys are to be transplanted because of the need to keep blood
circulating and filtered in order to prevent organ-damaging events like thrombosis, embolism, necrosis, DIC, or
cardiopulmonary or renal failure. Possible underlying causes include the Hs and Ts. Hypovolemia, Hypoxia,
Hydrogen ions (Acidosis), Hypothermia, Hyperkalemia or Hypokalemia, Hypoglycemia, Tablets or Toxins (Drug
overdose), Cardiac Tamponade, Tension pneumothorax, Thrombosis (Myocardial infarction), Thrombosis (Pulmonary
embolism), Trauma (Hypovolemia from blood loss)
72. Asystole epi, atropine, epi, atropine but don‘t shock.
73. Association of left axis deviation and cyanosis. Highly suggest tricuspid atresia. How to differentiate between TOF and
TA both have normal heart size, both have decreased vascular markings TOF have dilated Right atrium and right
74. Statins decrease mortality. In MI ACEI are only used when there is CHF, Ant. Wall MI, EF < 40%
75. Heparin prevent clot formation while thrombolytic don‘t prevent clot formation so give heparin in unstable angina
while give thrombolytic to MI. When thrombolytic and heparin are both contraindicated then what to do? Angioplasty.
76. When you use CCB? When you can‘t use BB or prinzmetal angina.
77. Immediate post MI cause of death? Arrythmia. So can we use prophylatically Lidocaine? No because it causes some
arrhythimas so don‘t change mortality.
78. You can use thrombolytic for upto 12 hours in MI while for stoke its upto 3 hours.
79. Measurement of EF most accurate method?or way is MUGA scan ( a nuclear ventriculogram )
80. BB reduces mortality more than ACEI.
81. Valselva maneuvor effect on heart? Decrease preload, decrese the venous return to the heart and so decrease preload.
Squatting effect on the heart. Increaese preload as squeezing the leg vein. Leg raising in the air is same as squatting so
increases preload. Preload reduction is like doing Valselva.
82. MC symptom of IHHS? SOB. HISS and MVP don‘t get diuretics but use BB Never use ACEI. Why BB are useful in
IHHS? Heart rate decrease and so heart fill more so obstruction decreases in HISS. MC symptoms of MVP? Panic
attack, pain palpataion. Small heart, Small ring and leaflet don‘t fit each other and become leaky. Large heart more fit
leaflet. MVP BB makes the heart bigger so it doesn‘t regurgitate.
83. Causes of restrictive heart disease? Sarcoidosis, Amyloidosis, hemochromatosis, Cancer and fibrosis.
84. Digoxin and verapamil are contraindicated in patient with Afib and WPWS.
85. Amiodarone S/E Pulmonary fibrosis, thyroid dysfunction, hepatotoxicity, corneal deposits, Skin reactions.
86. HTN + Hyperkalemia indicate secondary HTN. Causes includes: Primary hyperaldosteronism (MC), RVD, Diuretics,
Cushings, Bilateral Adrenal hyperplasia, renin secreting tumors.
87. Pericarditis EKG changes: Diffuse ST elevation with upward concavity at J point, No new Q wave, PR segment
elevation in aVR with PR depression in other leads.
88. Digoxin Toxicity: At therapeutic level (ST segment depression, T wave inversion, 1st
degree AV block) Tx? NO
TREATMENT. At Toxic level (Atrial flutter, A fib, Mobitz blocks, Atrial Tachycardia with variable AV block ( MC
EKG finding).Tx? yes treat. Initiate supportive therapy with oxygen, cardiac monitoring, and IV access. Activated
charcoal is indicated for acute overdose or accidental ingestion. Cholestyramine binds enterohepatically-recycled
digoxin and digitoxin, although no outcome studies have been performed. Gastric lavage increases vagal tone and may
precipitate or worsen arrhythmias. Consider pretreatment with atropine if gastric lavage is performed. The availability
of a digitalis-fab antibodies (Digibind) antidote usually renders gastric lavage unnecessary. Management of
dysrhythmias varies, depending on the presence or absence of hemodynamic instability, the nature of the arrhythmia,
the presence or absence of electrolyte disturbances, and the preferences of toxicology and/or cardiology consultants.
Bradyarrhythmias that are hemodynamically stable may be treated with observation and discontinuation of the drug.
Ensure proper hydration to optimize renal clearance of excess drug. GI binding agents (eg, charcoal, cholestyramine)
may be utilized to bind enterohepatically-recycled digitalis. Hemodynamically stable supraventricular arrhythmias may
be treated conservatively with observation and discontinuation of digoxin. In the setting of rate-related ischemia or
hemodynamic instability, Digibind is the treatment of choice. Short-acting beta-blockers (eg, esmolol) may be helpful
for supraventricular tachyarrhythmias with rapid ventricular rates, but advanced or complete AV block may be
precipitated. Calcium channel blockers are contraindicated because they may increase digoxin levels.
Hemodynamically unstable bradyarrhythmias respond best to Digibind. Atropine may be used for temporary adjuncts
because it improves AV nodal conduction. Cardiac pacing has been used successfully, but it can lower the fibrillatory
threshold and induce arrhythmias. PVCs, bigeminy, or trigeminy may be observed unless the patient is
hemodynamically unstable, in which case lidocaine may be effective. Ventricular tachycardia responds best to
Digibind. Lidocaine and phenytoin may be useful because they depress the enhanced ventricular automaticity without
significantly slowing AV conduction. Phenytoin may reverse digitalis-induced prolongation of AV nodal conduction.
Phenytoin has been shown to dissociate the inotropic and dysrhythmic action of digitalis, thus suppressing
digitalis-induced tachydysrhythmias without diminishing the contractile effects. In addition, phenytoin can terminate
supraventricular dysrhythmias induced by digitalis, whereas lidocaine has not been as effective. Lidocaine may be
given in boluses of 100 mg, according to advanced cardiac life support (ACLS) guidelines. If lidocaine is successful,
begin a maintenance infusion at 1-4 mg/min. Phenytoin has been administered in boluses of 100 mg every 5-10 minutes
up to a loading dose of 15 mg/kg. Avoid procainamide and bretylium. Asystole and ventricular fibrillation are very
89. Digibind is indicated; however, its effect is limited by poor cardiac blood flow. Nevertheless, the use of digoxin-fab
fragments has been associated with a 50% survival rate in isolated case reports. Quinidine, procainamide, and
bretylium are contraindicated. Both quinidine and procainamide worsen AV, SA, and His-Purkinje conductivity.
Additionally, quinidine reduces digoxin tissue binding and renal clearance, thereby increasing digoxin levels.
Bretylium can precipitate ventricular dysrhythmia. Cardioversion is relatively contraindicated because asystole or
ventricular fibrillation may be precipitated. Consider magnesium therapy as a temporizing antiarrhythmic agent until
fab fragments are available. It may be lifesaving when ventricular tachycardia or ventricular fibrillation is present.
Intravenous magnesium sulfate, 2 g over 5 minutes, has been shown to terminate digoxin-toxic cardiac arrhythmias in
patients with and without overt disease. Aside from successful replacement of intracellular magnesium, it also may act
as an indirect antagonist of digoxin at the supraphysiologic level.After an initial bolus of 2 g intravenously, a
maintenance infusion at 1-2 g/h is initiated. Monitor magnesium levels approximately every 2 hours. The therapeutic
goal is a level between 4 and 5 mEq/L. Correct electrolyte abnormalities, especially hypokalemia and
hypomagnesemia. Dysrhythmias may be reversed with correction of electrolyte imbalances. Treat hyperkalemia when
level is greater than 5.5 mEq/L. Calcium is not recommended to treat hyperkalemia in this setting because
ventricular tachycardia or ventricular fibrillation may be precipitated. This is based on the fact that intracellular calcium
levels are already high in the setting of digoxin toxicity. However, anecdotal case reports and animal studies have been
published that refute the dangers of calcium administration. Unless the patient is in extremis, other measures should be
preferentially used to treat hyperkalemia. Sodium bicarbonate and/or glucose and insulin are indicated. Treatment with
digoxin-fab fragments is indicated for hyperkalemia with K+
level greater than 5 mEq/L. Kayexalate (0.5 g/kg PO) also
is helpful in binding potassium and enterohepatically-recycled digitalis. However, digoxin-induced hyperkalemia
reflects an extracellular shift, not an increase in total body potassium. Caution is indicated when using Kayexalate
concurrently with insulin/glucose/bicarbonate and/or Digibind because hypokalemia may be precipitated, which may
worsen clinical toxicity. Digoxin-fab fragments (Digibind) are generally indicated for the following: Dysrhythmias
associated with hemodynamic instability. Altered mental status attributed to digoxin toxicity. Hyperkalemia with
greater than 5 mEq/L. Serum digoxin level greater than 10 ng/mL in adults at steady state (ie, 6-8 h post acute
ingestion or at baseline in the clinical setting of chronic toxicity). Ingestion greater than 10 mg in adults (40 X 0.25 mg
tablets) or greater than 0.3 mg/kg in children.
90. BB CI? ABCDPR (asthma, bradycardia, block, 2, 3, COPD, DM, Depression, Pulmonary edema, PVD, Raynaud
Phenomenon). CCB CI? BC (Block 2, 3, CHF with systolic dysfunction). ACEI CI? HP (Hyperkalemia, Pregnancy).
Diuretics CI? Drugs allergy, Gout. HOCM. BIT? ECHO when echo fail to diagnose then? MRI. When to start ACEI in
stable Angina pt? DM, HTN, Low EF <50%.
91. Hypotension + bradycardia Dx? Heart block.
92. Right Coronary Artery (inferior and posterior segment of the heart) EKG changes seen in: II, III, aVF. Circumflex
Artery (Anterolateral region of the heart) EKG changes seen in: V5, V6 and I, aVL. Left Anterior Descending LAD:
(Anterolateral & anteroapical region of the heart, EKG changes seen in: V1-V4. Left Coronary Artery: Encompass
region supplied by LAD & circumplex, EKG Changes: V5-V6 and I and aVL. Posterior Descending Artery PDA:
Posterior aspect of heart: EKG changes: Tall R waves in V1-V2.
93. Septic shock: Hyperdinamic circulation, elevated CO, Low SVR, RAP, PCWP and normal MVO2. Septic shock is a
type of distributive shock having normal MVO2. Other types of distributive shock neurogenic and hypovolumic have
decreased MVO2 (mixed venous Oxygen). In septic shock right heart and left heart pressure are both low.
94. In constrictive pericarditis and Cardiac tamponade Right and left heart pressures are both equal. Constrictive peri
carditis has early S3 called pericardial knock.
95. Which one will more decrease the risk of abdominal aortic aneurysm from enlarging? A. Stop smoking B. Blood
pressure control. There are no medications you can take to prevent an aortic aneurysm. Researchers think that statin
medications and some antibiotics can slow the growth of small aortic aneurysms. There's also some evidence that the
angiotensin receptor blocker losartan (Cozaar) may prevent aneurysm formation. For now the best approach to prevent
an aortic aneurysm is to keep your blood vessels as healthy as possible. That means taking these steps: Keep your blood
pressure under control. Don't smoke. Get regular exercise. Reduce cholesterol and fat in your diet. It's especially
important to quit using tobacco because smoking or chewing tobacco can increase the chances your aneurysm will
96. Abdominal aortic aneuryzm: less then 4---usg annually, less then 5--usg 6 months, more then 5, tender mass or increase
in size more then .5cm in 6 months--refer for surgery urgently.
97. Heart Failure Diagnosis. MAJOR Critaria: PPROTIC ( Paroxysmal nocturnal dyspnea, Pulmonary rales, Raised JVP,
Orthopnea, Third heart sound, Increased cardiac silhouette, Congestion pulmonary vascular ). MINOR Critaria:
CHEDET (Cough nocturnal, Hepatomegally, Effusion pleural, Dyspnea on exertion, Edema lover extremity bilateral,
98. Causes of Acute Heart Failure‖ PICT (Papillary muscle rupture, Infective endocarditis, Chordien Tendine rupture,
Trauma to chest wall). Now how to differentiate between papillary muscle and Chordien tendine? Papillary muscle
rupture has MI history.
99. Where we directly use Warfarin without using the heparin? Atrial Fibrillation.
100. Which antihypertensive drugs reduce the risk of DM2? ACEI. Which antihypertensive increased the risk of DM? BB
101. Coronary angiography has iodine in it so it can cause thyrotoxicosis.
102. Syncope: Neurocardiogenic (prodromal symptoms, nausea, Light headedness, pallor, diaphoresis.) Cardiogenic
(Palpatation + Risk Factor for syncope). Autonomic Neuropathy (Postural Hypotension). Neurological (Due to
atherosclerosis h/o Focal neurological deficits.)
103. LA Statin which increases Fibrinogen? Lovastatin, Atorvastatin while Sim and Pravastation have no
Effect on Fibrinogens. (Fibrinogen is increased in LA coz of best and most populous city in CA )
104. Smoking increases Fibrinogen level but if u stop smoking it will take 20 years to be effective.
105. PVD medication!!!! Cilostazol and pentoxiphylline
106. MC post operative complication of major vascular surgery is? MI
107. HEART BLOCK: 1st
just talk about PR interval which is increased > 200msec. 2nd
two types. Both talk about PR
interval and a drop beat so how to differentiate between the two? Mobitz I = PR interval increases gradually until a
drop beat occur. Mobitz II= No PR interval increase but a drop beat occurs. 3rd
Complete block (Total Block) with no
relation to P wave and QRS complex.
108. Systolic dysfunction (S3, dec EF, Ischemic heart disease. Tx? Dec after load with ACEI, positive inotropic agent like
digoxin ) Diastolic dysfunction ( S4, Normal EF, MCC hypertrophy of the LV due to long standing HTN, Tx. Don‘t
decrease preload with diuretics, BB to slow heart rate and to increase the CO)
109. On cardiac exam which is suggestive of Cardiac ischemia? A) Early diastolic murmur at the base. B) A late systolic
murmur at the apex. C) Mid-systolic click. D) Pericardial knock. E) Pulsus paradoxus: Physical: For most patients with
stable angina, physical examination findings are normal. Diagnosing secondary causes of angina, such as aortic
stenosis, is important. A positive Levine sign (characterized by the patient's fist clenched over the sternum when
describing the discomfort) is suggestive of angina pectoris. Look for physical signs of abnormal lipid metabolism (eg,
xanthelasma, xanthoma) or of diffuse atherosclerosis (eg, absence or diminished peripheral pulses, increased light
reflexes or arteriovenous nicking upon ophthalmic examination, carotid bruit). Examination of patients during the
angina attack may be more helpful. Useful physical findings include third and/or fourth heart sounds due to LV systolic
and/or diastolic dysfunction and mitral regurgitation secondary to papillary muscle dysfunction. Pain produced by
chest wall pressure is usually of chest wall origin.
110. Phlegmasia cerulea dolens (literally: painful blue edema) is an uncommon severe form of deep venous
thrombosis which results from extensive thrombotic occlusion (blockage by a blood clot) of the major and
the collateral veins of an extremity. It is characterized by sudden severe pain, swelling, cyanosis and edema of the
affected limb. There is a high risk of massive pulmonary embolism, even underanticoagulation. Foot gangrene may
also occur. An underlying malignancy is found in 50% of cases. This phenomenon was discovered by Jonathan Towne,
a vascular surgeon in Milwaukee, who was also the first to report the "white clot syndrome" (Now called HIT= Heparin
induced thrombocytopenia). Two of their HIT patients developed Phlegmasia cerulea dolens that went on to become
gangrenous. Phlegmasia alba dolens (also colloquially known as milk leg or white leg) is part of a spectrum of diseases
related to deep vein thrombosis. Historically, it was commonly seen during pregnancy and in mothers who have just
given birth. In cases of pregnancy, it is most often seen during the third trimester, resulting from a compression of the
left common iliac vein against the pelvic rim by the enlarged uterus. Today, this disease is most commonly (40% of the
time) related to some form of underlying malignancy. Hypercoaguability (a propensity to clot formation) is a
well-known state that occurs in many cancer states. The disease presumably begins with a deep vein thrombosis that
progresses to total occlusion of the deep venous system. It is at this stage that it is called phlegmasia alba dolens. It is a
sudden (acute) process. The leg, then, must rely on the superficial venous system for drainage. The superficial system is
not adequate to handle the large volume of blood being delivered to the leg via the arterial system. The result is edema,
pain and a white appearance (alba) of the leg. The next step in the disease progression is occlusion of the superficial
venous system, thereby preventing all venous outflow from the extremity. At this stage it is calledphlegmasia cerulea
dolens. The leg becomes more swollen and increasingly more painful. Additionally, the edema and loss of venous
outflow impedes the arterial inflow. Ischemia and, hence, gangrene are the ultimate dreaded consequence. Phlegmasia
alba dolens is distinguished, clinically, from phlegmasia cerulea dolens in that there is no ischemia. "Phlegmasia alba
dolens" literally means "painful white edema".It received the name "milk leg" because it was once thought to be caused
by the metastasis of milk. The incidence of this disease is not well reported.
111. What should be done about an elevated homocysteine level that persists despite administration of high-dose folic acid
and high blood levels of folic acid? Response from Erica Brownfield, MD. High homocysteine levels are associated
with an increased risk of cardiovascular and cerebrovascular disease. Hyperhomocysteinemia can be caused by several
mechanisms: (1) genetic defects in the enzymes involved in the metabolism of homocysteine, (2) nutritional
deficiencies in vitamin cofactors, or (3) some chronic medical conditions and drugs. Smoking may increase
homocysteine levels in the blood. In the absence of known cardiovascular or cerebrovascular disease, it is controversial
whether or not to treat patients with elevated homocysteine levels. There is no clear evidence for treating patients who
do not have severe hyperhomocysteinemia in the absence of cardiovascular or thrombotic disease.
conflicting data on the efficacy of supplementation aimed at lowering homocysteine levels to prevent vascular events
and death in patients with established vascular disease.[2-4]
For patients who are treated, the treatment should target the
underlying cause, if known. In general, a diet rich in fruits, vegetables, and low-fat dairy products as well as low in
saturated and total fat can help to decrease serum homocysteine. For patients with known cardiovascular disease, it is
generally recommended to treat with folic acid (1 mg/day), vitamin B6 (10 mg/day), and vitamin B12 (0.4 mg/day).
Folic acid can be increased up to 5 mg/day to reach a goal of lowering homocysteine levels below 15 mmol/L. In
patients refractory to 5 mg/day of folic acid, 750 mg twice daily of trimethylglycine have been used, but there are only
limited data demonstrating efficacy.
It is known that trimethylglycine enhances the methylation metabolism of
homocysteine. Although treating hyperhomocysteinemia can be very important, it should go without question that the
more significant cardiovascular risk factors, such as diabetes, hypertension, hypercholesterolemia, and tobacco use,
must also be addressed.
112. PVD: Pt present with symptom then first do ABI if its <0.9 is is positive for ischemia. If ABI is normal and pt has
symptoms then perform ABI before and after exercise on a treadmil. Cilostazol is the best drug for PVD. Its MOA is
platelet aggregation inhibition because it is phosphodiasterase inhibitor and arteolar dilatation.
113. Acute compartment syndrome when seen then measure tissue pressure. Normal threshold is <30mmHg which warrants
1. Candidal diaper rash (tomato red plaques and satellite papules candidal intertrigo and perineal infection) & diaper
dermatitis (same except spares genitor-crural fold) Tx. Rash (antimycotic cream I e Clotrimazole and nystatin) and for
dermatitis its zinc oxide cream and petroleum ointment. These infections are common in those children who have used
antibiotic recently. Antibiotic destroy the normal bacterial flora which favors fungal infection.
2. Atopic dermatitis also called eczema or itch that rash, hallmark is pruritis and relapsing nature (rash involve the face
and scalp. Scaly, dry checks. TX topical steroid and Calcineurin Inhibitors Such as Tacrolimus and
Pimecrolimus.Poison ivy and Poison Oak, vesicular, linear streak like. Topical steroid usually don‘t work.
1. Herpez zoster prevention: depend on patient location. If at community just cover the lesion because it is spread by
direct contact with the lesion while in hospital strict isolation until all lesion have crusted.
2. Tinea versicolor: macule with varying color (yeast inhibit pigment tranfer to keratinocytes).
3. Erythema toxicum neunatorum: Noncontagous, occur in term infant on 1st
day of life. It begins on the face and
torso and proximal extremities. It spares the sole and feet.inflammatory macule and pustule. With wright stain you can
see the numerous eosinophills. In contrast to this neonatal acne appears in 2nd
week of life and is pustular fascial
eruption. Some of these lesion has fungal organism. No treatment for both of these conditions.
4. mild.... papules, psutule..............local
moderate..... nodularcystic.......local + antibiotiss
severe.....nodules , scarring........isoretenoid
5. Basal cell carcinoma rare before age 40 years.
6. Seborrheic Keratosis rare before age 30.
7. DD of melanoma::: Seborrheic keratosis "Stuck-on" appearance, symmetric, often multiple. Traumatized or irritated
nevus Returns to normal appearance within 7 to 14 days. Pigmented basal cell carcinoma Waxy appearance,
telangiectasias. Lentigo Prevalent in sun-exposed skin, evenly pigmented, symmetric. Blue nevus Darkly pigmented
from dermal melanocytes, no history of change. Angiokeratoma Vascular tumors, difficult to distinguish from
melanoma. Traumatic hematoma May mimic melanoma but resolves in 7 to 14 days. Venous lake Blue, compressible,
found on ears and lips. Hemangioma Compressible, stable. Dermatofibroma Firm growths of fibrous histiocytes,
"button-hole" when pinched. Pigmented actinic keratosis Sandpapery feel; sun-exposed area. Melanoma types: SNLA (
Superficial MC in whites, Nodular 2nd
MC exophytic nodule, Lentigo Elderly, hands feet which are sun exposed areas,
Acral MC in black, occuars on palms, soles and nail areas. For high risk patient with mestastasis of melanoma we use
interferon alpha 2b as an adjuvent therapy.
8. treatment for a pregnant lady in first trimester with
a. CANDIDIASIS: Imidazoles are best but pregnant women may need longer (7 not 4 day) courses. Thrush is a
common vaginal infection in pregnancy causing itching and soreness. There is no evidence that this yeast
infection harms the baby. Antifungal creams are effective. Imidazoles (such as clotrimazole) are more
effective than older treatments such as nystatin and hydrargaphen. Longer courses (7 days) cured more than
90% of women whereas standard (4 day) courses only cured about half the cases.
BV: Clindamycin 300 mg po tid X 7 days can be used in first trimeste, demonstrated effective
Topical clindamycin cream when oral is not tolerated.
Trichomoniasis: If you test positive for trich you will probably only be treated if your symptoms are
bothersome and persistent. The drug metronidazole is the most effective cure for Trichomoniasis. However,
some studies show that metronidazole actually increases the risk of pre-term or premature birth for your
baby. A study performed by the National Institute of Child Health and Human Development found that
metronidazole use in pregnancy can significantly increase the chance of pre-term labor. To date, studies are
inconclusive on the actual risks of using metronidazole during pregnancy. If your symptoms are bad, you
may be offered clotrimazole vaginal tablets as an alternative treatment. These are inserted inside your vagina
once daily for 7 days.
Common these three infections need 7 days treatment :)
9. Scaling plaque with indistant margin (Seborrhic Dermatitis) Scaling plaque with distant margin (Psoriasis).
10. Psoriasis treatment: Localized Psoriasis (Topical steroids), Think plaque on extensor surface (High potency
betamethasone), Face and intertrigous area (Low potency hydrocortisone), When >30% body area involved then?
Use phototherapy with IV radiation. Psoriasis arthritis (Methotrexate).
11. Aktinic Keratosis: Slowly growing, reddish brown skin lesion: premalignant condition for SCC. Actinic keratoses
are lesions on the outer skin layer caused by too much exposure to the ultraviolet rays of sunlight. They are also
the beginnings of skin cancer, most often appearing after age 40. In some areas where climate is mild year-round
like Florida and California -- these lesions appear in much younger people, even teenagers. People with fair skin,
blond or red hair, and blue or green eyes are most at risk of developing these rough, scaly "bumps." A history of
burning rather than tanning also increases risk. If not treated, these bumps can develop into a more serious form
of skin cancer.
12. This seborrheic keratosis is darker colored. Seborrheic keratoses are very common lesions which tend to appear
after age 30 and are increasingly common in older age groups. The temples, the rest of the face, and the back are
common locations. Medically, seborrheic keratoses are usually insignificant, but can be treated (see treated
image) if repeatedly irritated, or for cosmetic reasons. Seborrheic keratoses are not thought to be related to
either seborrheic dermatitis or
15- Keratoacanthoma: A keratoacanthoma is a rapidly evoling tumor of the skin with a ―volvano-like appearance,
rising sharply from the surrounding skin as a smooth edge tumor. Centrally, within the cone of the ― volcano‘ is rough
keratotic tissue. Keratoacanthomas usually spontaneously resolve within eight weeks although they may continue to
enlarge for months. When they resolve there is usually a scar remaining. Multiple keratoacanthomas of
Fergusson-Smith is a variant. Diagnosis is made by histology.TX? Keratoacanthomas should be surgically removed.
Squamous cell carcinoma can clinically resemble keratoacanthomas. Incisional biopsy is often inadequate to
differentiate keratoacanthoma from rapidly growing squamous carcinoma.
16- Verruca Vulgaris: Benign cutaneous papilloma (common wart). Single or grouped, rough keratotic papules,
nodules, or plaques
17-basal cell carcinoma can take several forms: Small, translucent growth with rolled edges that may be
pigmented (brown) or have small blood vessels on the surface. Open sore that bleeds, heals, and then repeats the
cycle. Cluster of slow-growing, shiny pink or red lesions that are slightly scaly and bleed easily. Flat or slightly
depressed lesion that feels hard to the touch; may be white or yellow and have indistinct borders. Waxy scar that
is skin-colored, white, or yellow.
Basal cell Carcinoma.
18- This nonmelanoma skin cancer may appear as a firm red nodule, a scaly growth that bleeds or develops a
crust, or a sore that doesn't heal. It most often occurs on the nose, forehead, ears, lower lip, hands, and other
sun-exposed areas of the body. Squamous cell carcinoma is curable if caught and treated early. If the skin cancer
becomes more advanced, treatment will depend on the stage of cancer.
19- Pityriasis rosea is a skin rash that often sweeps out from the middle of your body, with a shape that resembles
drooping pine-tree branches. Pityriasis (pit-ih-RI-uh-sis) rosea usually begins as one large spot on your chest,
abdomen or back and then spreads. Although pityriasis rosea has a distinctive appearance once the rash spreads,
in its early stages you may confuse pityriasis rosea with other skin disorders. Pityriasis rosea can affect any age
group, but commonly affects older children and young adults. It usually goes away on its own, but may last for
several weeks. Before it disappears, pityriasis rosea may make you mildly uncomfortable, but there are steps you
can take to relieve your discomfort.
20- Tinea versicolor (TIN-ee-uh vur-si-KUL-ur), also called pityriasis versicolor, is a common fungal infection of
the skin. The fungus interferes with the normal pigmentation of the skin, resulting in small, discolored patches.
Tinea versicolor is most common in teens and young adults. Sun exposure may make tinea versicolor more
apparent. Antifungal creams, lotions or shampoos can help treat tinea versicolor. But even after successful
treatment, skin color may remain uneven for several weeks until repigmentation occurs, and tinea versicolor may
return, especially in warm, humid weather. TX. Clotrimazole topical.
21- Intralesional conticosteroid is used for keloid scar and alopecia areata.
22- Atopic dermatitis (eczema) is an itchy inflammation of your skin. It's a long-lasting (chronic) condition that may be
accompanied by asthma or hay fever. Eczema is most often seen in infants and children, but it can continue into adulthood
or first appear later in life. Eczema may affect any area, but it classically appears on your arms and behind the knees. It
tends to flare periodically and then subside. The cause of atopic dermatitis, or eczema, is unknown, but it may result from
a malfunction in the body's immune system. Self-care measures, such as avoiding soaps or other irritants and applying
creams or ointments, can help relieve itching.
23- Lichen planus (LP) is a relatively common disorder affecting middle-aged individuals. The average age of onset is
about 50 years. It is evenly distributed world wide and affects females more than males. Clinically, the disorder presents
as pruritic, flat-topped, violaceous, polygonal papules most commonly on the flexural surfaces. The mucous membranes
are involved in up to 65 percent of cases and occasionally nails can be affected as well. If biopsied, histopathologic
examination shows a band-like infiltrate of lymphocytes at the dermal-epidermal junction. Other salient features include
hyperkeratosis, wedge-shaped hypergranulosis, acanthosis with saw-toothed rete ridges, and vacuolar degeneration of
the basal layer. Civatte bodies (colloid or cytoid bodies) are present at the dermal-epidermal junction and in the papillary
dermis. A variety of treatment modalities has been used to relieve pruritus and induce remission of lichen planus. These
modalities included topical and systemic steroids, dapsone, cyclosporine, retinoids, methotrexate, azathioprine,
narrow-band ultraviolet-B phototherapy and psoralen plus ultraviolet A (PUVA).
24- Acne vulgaris: The common type of acne is called acne vulgaris. It is a condition that mainly affects adolescents but
may persist or even become more severe in adulthood. Most, but not all, acne patients have oily skin (seborrhoea).
Clinical featuresAcne vulgaris may occur on the face, chest, back and sometimes even more extensively. Several types of
acne spots occur, often at the same time. Non-inflammatory lesions: Open comedones (blackheads), closed comedones
(whiteheads), uninflamed nodules (sometimes called cysts). Inflammatory lesions: Papules (small red bumps). Pustules
(white or yellow ‘squeezable’ spots). Inflamed nodules (large red lumps). Secondary lesions: Excoriations (picked or
scratched spots). Erythematous macules (red marks from recently healed spots, mostly in fair skin). Pigmented macules
(dark marks from old spots, mostly in dark skin), Scars. Individual acne lesions usually last less than two weeks but the
deeper papules and nodules may persist for months.
Biochemically Speaking, Acne Is Easy to Understand: Testosterone (an androgen hormone) targets the skin and
sebaceous glands where sebum is produced. Testosterone combines with the enzyme, 5alpha-reductase, to produce
dihydrotestosterone, which stimulates the sebaceous glands to produce increased volumes of sebum. Sebum is expelled
out of the follicular tube. Propionibacterium acnes (P. acnes) and other bacteria on the skin and within the follicles
produce bacterial lipases (enzymes) that move into the follicle openings and convert sebum into free fatty acids, which
irritates the follicle linings. This irritation causes excessive production of cells and cellular debris, which blocks the
follicles and traps P. acnes inside. The P. acnes bacteria inside the blocked follicles breed and produce acne
infections. Infections grow and inflame the skin. Macrophage cells produce inflammatory histamines that cause the
skin to become red, puffy and painful. This causes more follicle blockage and promotes more acne vulgaris
infections. In the case of acne vulgaris, the infections may not rise to the surface where the infection and its waste can be
Acne grading: Acne may be classified as mild, moderate or severe1. Comedones and inflammatory lesions are usually
Mild acne: <20 comedones, <15 inflammatory lesions. Or, total lesion count <30
Moderate acne: 20-100 comedones, 15-50 inflammatory lesions, or, total lesion count 30-125
Severe acne: >5 cysts, Total comedo count >100, Total inflammatory count >50, Or total lesion count >125.
Many dermatologists assess the severity of a patient's acne more precisely by using a grading scale, such as the one
developed by the Leeds' group. The inflammatory lesions are compared with a set of standard photographs to determine
the grade, which may be 1 (very mild) to 12 (exceptionally severe). In clinical trials evaluating acne treatment, the
numbers of uninflamed and inflamed lesions are carefully counted at regular intervals. It is remarkably difficult to count
consistently. Treatment. Which treatment is best depends on the patient's age and sex, the extent and the severity of the
acne. General principles of treatment
Acne can be effectively treated, although response may sometimes be slow.
Where possible, avoid excessively humid conditions such as a sauna, working in an unventilated kitchen or
If you smoke, stop. Nicotine increases sebum retention and increased scale within the follicles,
forming comedones (blackheads and whiteheads).
Minimise the application of oils and cosmetics to the affected skin.
Abrasive skin treatments can aggravate both comedones and inflammatory lesions.
Try not to scratch or pick the spots.
Exposure to sunlight filtered through window glass can help – see information about lasers, lights and acne. To
avoid sunburn, protect your skin outdoors using a sunscreen and protective clothing.
No relationship between particular foods and acne has been proven. However, reports suggest low glycaemic
and low dairy diet are helpful for some people.
Management of mild acne: Most patients with mild acne can be treated with topical treatment (gels, solutions
and lotions) that can be obtained over-the-counter in New Zealand without prescription. Most people just use
topical agents for facial skin as they can be difficult to apply to one's back. Extra vitamins and minerals have not
been proved to help.
Wash affected areas twice daily with a mild cleanser and water or an antiseptic wash.
Acne products should be applied to all areas affected by acne, rather than just put on individual spots.
A thin smear should only be applied to dry clean skin at nighttime.
Acne products may work better if applied in the morning as well.
They often cause dryness particularly in the first 2-4 weeks of use. This is partly how they work. The skin usually
adjusts to this.
Apply an oil-free moisturizer only if the affected skin is obviously peeling.
Avoid applying oily cosmetics such as foundation or sunscreen.
It may take several weeks or even months to see convincing improvement.
Discontinue using product if severe irritation results. See your doctor for advice.
Suitable topical agents for mild acne that can be obtained without prescription include:
Antiseptic washes (Acnederm wash™, Benzac™ AC Wash, Dalacin™ T Prewash, Oxy™ Daily Skin Wash)
Mild salicylic acid preparations to exfoliate and unplug the follicles (Neutrogena® Oil-free Acne Wash and many
Benzoyl peroxide cream / lotion / gel (PanOxyl™ Acne Gel, Brevoxyl™ Cream, Oxy-10™, Clearasil™ Ultra Acne
Cream, Benzac AC Gel)
Azelaic acid (Skinoren™ cream, Acnederm™ medicated lotion)
Hydrogen peroxide in stabilised cream (Crystacide®)
Tea tree oil products
Topical agents for mild acne which require prescription include:
Antibiotics, such as clindamycin solution (Topicil™) or erythromycin solution (Stiemycin™) and gel (Eryacne™)
are best used with benzoyl peroxide or azelaic acid to reduce the chance of antibiotic resistance.
Retinoids i.e. tretinoin (ReTrieve™, Retin-A™), isotretinoin (Isotrex™), adapalene (Differin™).
Combination prescription topicals include clindamycin / benzoyl peroxide (Duac™) and adapalene / benzoyl peroxide gel
Blue light acne treatment is a new procedure recently found to be safe and helpful for mild to moderate acne.
See your doctor or dermatologist for advice if your pimples fail to clear up within six weeks or you have severe acne.
Management of moderately severe acne
Treatment for moderately severe acne usually includes topical agents. In addition, a doctor or dermatologist may
prescribe an oral medication, usually for at least six months.
Suitable oral medications include:
Antibiotics such as tetracycline, minocycline, doxycycline or erythromycin
In females, oestrogens and antiandrogens such as Diane 35™/Estelle 35™ or spironolactone
Some patients are helped by nonsteroidal anti-inflammatory agents such as ibuprofen or naproxen
For resistant or persistent acne, oral isotretinoin may be more suitable
See your doctor or dermatologist for advice if your skin problem fails to improve within three months or you have severe
Management of severe acne
Treatment for severe acne requires oral treatment. Patients should be under the care of a dermatologist.
Many patients will be treated with oral isotretinoin.
If this is not suitable, the following may be used:
High dose oral antibiotics for six months or longer
In females, especially those with polycystic ovary syndrome, oral antiandrogens such as oestrogen/cyproterone
or spironolactone may be suitable long term. Systemic corticosteroids are sometimes used for their
antiandrogenic effect. Flutamide and finasteride also been reported to be of benefit in hyperandrogenic women.
At this time, these medicines are registered for treatment of prostatic cancer (and in the case of finasteride,
for androgenetic alopecia) in males only, in New Zealand.
Physical treatments for acne
Sunlight is anti-inflammatory and can help briefly. However, exposure to ultraviolet radiation results in ageing
skin and can eventually lead to skin cancer.
Cryotherapy (freezing treatment) may be useful to control new nodules.
Intralesional steroid injections can be used to shrink older nodules.
Comedones can be expressed or removed by cautery or diathermy.
Microdermabrasion can help mild acne.
Lasers and other light systems appear helpful for acne. Treatment is often delivered twice weekly for four
weeks. The effect may be enhanced by use of a photosensitising agent (photodynamic therapy).
Note: X-ray treatment is no longer recommended for acne as it may cause skin cancer.
25- Eleven major symptoms of rosacea with color photos: Facial flushing, Facial redness, Facial telangiectasia, Facial
skin hyper-reactivity, Lumpy-bumpy facial skin, Facial papules, Facial pustules, Facial burning sensations, Facial
swelling, Rhinopyma, Ocular symptoms.
26- Butterfly rash: A red, flat facial rash over the bridge of the nose. Over half of patients with systemic lupus
erythematosus (SLE) develop this characteristic rash. Because of its shape, it is frequently referred to as the "butterfly
rash" of lupus. The butterfly rash of lupus is typically painless and does not itch. Along with inflammation in other organs,
the butterfly rash of lupus can be precipitated or worsened by exposure to sunlight, a condition called photosensitivity.
The photosensitivity can be accompanied by a worsening of inflammation throughout the body, causing a "flare" of the
disease. A "butterfly" rash can also occur in other conditions such as rosacea.
27- Evaluating the Febrile Patient with a Rash
HARRY D. MCKINNON, JR., MAJ, MC, USA, and
THOMAS HOWARD, COL, MC, USA
Dewitt Army Community Hospital, Fort Belvoir, Virginia
The differential diagnosis for febrile patients with a rash is extensive. Diseases that present with fever and rash are
usually classified according to the morphology of the primary lesion. Rashes can be categorized as maculopapular
(centrally and peripherally distributed), petechial, diffusely erythematous with desquamation, vesiculobullous-pustular
and nodular. Potential causes include viruses, bacteria, spirochetes, rickettsiae, medications and rheumatologic diseases.
A thorough history and a careful physical examination are essential to making a correct diagnosis. Although laboratory
studies can be useful in confirming the diagnosis, test results often are not available immediately. Because the severity of
these illnesses can vary from minor (roseola) to life-threatening (meningococcemia), the family physician must make
prompt management decisions regarding empiric therapy. Hospitalization, isolation and antimicrobial therapy often must
be considered when a patient presents with fever and a rash. (Am Fam Physician 2000;62:804-16.)
Evaluating the patient who presents with fever and a rash can be challenging because the differential diagnosis is
extensive and includes minor and life-threatening illnesses. In addition, the clinical picture can vary considerably, and the
family physician may need to quickly decide about initiating empiric therapy or isolation. This article reviews common
diagnoses for fever and a rash and suggests a logical approach to obtaining the correct diagnosis.1-3
A detailed history can be quite helpful in identifying the cause of fever
and a rash. A history of recent travel, woodland or animal exposure,
drug ingestion or contact with ill persons should be noted. The time of
year can be a clue to certain diagnoses.2-4
A complete medical history can help to determine whether the patient is
at increased risk for specific conditions associated with valvular heart
disease, sexually transmitted diseases or immunosuppression from chemotherapy. Immune status is particularly
A history of recent travel, woodland or animal
exposure, drug ingestion or contact with ill
persons should be noted when the family
physician evaluates a patient who has fever
and a rash.
important because many of the diseases that result in fever and a rash present differently in immunocompromised
Details about the rash should include site of onset, rate and direction of spread, presence or absence of pruritus, and
temporal relationship of rash and fever.2-5 It is also important to know whether any topical or oral therapies have been
A basic understanding of the various types of rashes is essential in making an accurate assessment and determining the
severity and acuteness of the patient's illness. Brief descriptions of common primary skin lesions are presented in Table
The physician should identify the primary lesion but also note the presence of secondary lesions. Important features
include the distribution, configuration and arrangement of the lesions.2
In addition to evaluating the patient's vital signs and general appearance, the physician should look for the following:
signs of toxicity, adenopathy, oral, genital or conjunctival lesions, hepatosplenomegaly, evidence of excoriations or
tenderness, and signs of nuchal rigidity or neurologic dysfunction.2,4
Common Primary Skin Lesions
Macule Circumscribed area of change in normal skin color, with no skin elevation or depression; may be any size
Papule Solid, raised lesion up to 0.5 cm in greatest diameter
Nodule Similar to papule but located deeper in the dermis or subcutaneous tissue; differentiated from papule by
palpability and depth, rather than size
Plaque Elevation of skin occupying a relatively large area in relation to height; often formed by confluence of papules
Pustule Circumscribed elevation of skin containing purulent fluid of variable character (i.e., fluid may be white,
yellow, greenish or hemorrhagic)
Vesicle Circumscribed, elevated, fluid-containing lesion less than 0.5 cm in greatest diameter; may be intraepidermal
or subepidermal in origin
Bulla Same as vesicle, except lesion is more than 0.5 cm in greatest diameter
Information from Fitzpatrick TB, et al. Color atlas and synopsis of clinical dermatology: common and serious diseases. 3d
ed. New York: McGraw-Hill, Health Professions Division, 1997, and Habif TP. Clinical dermatology: a color guide to
diagnosis and therapy. 3d ed. St. Louis: Mosby, 1996.
Laboratory data are not usually available during the initial evaluation. The complete blood count with differential, an
erythrocyte sedimentation rate, a chemistry panel, liver function tests, and blood and urine cultures may prove useful in
identifying organisms or disease processes.1
Aspirates, scrapings and pustular fluid may be obtained for Gram staining and culture. When a herpes simplex virus
infection is suspected, a Tzanck test may be performed by unroofing a lesion and taking a scraping of the lesion base.
Biopsy samples should be obtained from nonhealing or persistent purpuric lesions. Biopsy of inflammatory dermal
nodules and ulcers should also be considered.1
Specific diagnoses that may be confirmed histologically include Rocky Mountain spotted fever, herpetic infections,
systemic lupus erythematosus, erythema multiforme, allergic vasculitis, secondary syphilis and deep fungal infections.1,6,7
Although serologic tests are not helpful in the acute setting, they can be used to confirm or support the diagnosis of
conditions such as systemic lupus erythematosus, syphilis, rheumatoid arthritis and human immunodeficiency virus
Diseases that present with fever and rash are summarized in Table 21,2 and discussed by rash type in the following
Diseases Presenting with Fever and Rash
Disease Etiology Description of rash Epidemiology Diagnostic clues Basis for diagnosis
Rubeola Measles virus Macular-papular rash
that may become
confluent; begins on
face, neck and shoulders
Most common in
children 5 to 9
years of age,
of symptoms of
inferiorly; fades in 4 to 6
persons coryza, bark-like
fever; Koplik's spots
exanthem on fourth
febrile day; late
winter through early
Rubella Rubella virus Pink macules and
papules that develop on
forehead and spread
inferiorly and to
extremities within one
day; fading of macules
and papules in reverse
order by third day
on soft palate
spots); in adults:
symptoms of mild
Human parvovirus B19 Begins as classic
bright-red facial rash
("slapped cheek") and
progresses to lacy
reticular rash; may wax
and wane for 6 to 8
Children 3 to 12
years of age
Can present as
in adults; prodrome
of fever, anorexia;
resolution of fever
Roseola Human herpes-virus 6 Diffuse maculopapular
months to 3
years of age
Fever lasting 3 to 4
within 2 to 3 days by
the rash, which
several days; almost
always a self-limited
relationship of fever
followed by rash is
helpful in making the
Lyme disease Borrelia burgdorferi Macule or papule at site
of tick bite, progressing
All ages at risk
for tick exposure
in endemic areas
History of tick
erythema migrans Borrelia
Idiopathic in 50 percent of
cases (see Table 3)
developing into papules
with central vesicles or
bullae; common on
dorsa of hands, palms,
soles, arms, knees, penis
and vulva; often
bilateral and symmetric
Adults 20 to 30
years of age;
more often than
Major and minor
forms; major form
always with mucous
usually the result of
drug reaction; minor
Secondary syphilis Treponema pallidum Various presentations;
brownish- red or pink
macules and papules;
generalized eruption or
localized eruption on
head, neck, palms or
soles; condyloma lata
adults 15 to 49
years of age;
more often than
Develops 2 to 10
presents with or
without fever; may
may have recurrent
Neisseria meningitidis Variety of lesions but,
distributed on the trunk
(although the lesions
can be located
anywhere); petechiae on
months to 1 year
Acutely ill patient;
in more than 50
percent of patients
N. meningitidis Intermittent
often on a painful joint
or pressure point; may
have nodules on calves
Same as for
may recur for weeks
or months, with
average duration of
8 weeks; may
progress to acute
Rickettsia rickettsii Rash evolving from pink
macules to red papules
and finally to petechiae;
rash beginning on wrists
and ankles and
involvement of palms
and soles late in disease
abrupt; fever, severe
fourth day of illness;
may have relative
Scarlet fever Beta-hemolyticStreptococcus
beginning on trunk and
spreading to extremities,
flushed face with
perioral pallor; rash
fading in 4 to 5 days and
Children Acute infection of
tonsils or skin; linear
(Pastia's sign); rash
appearing 2 to 3
days after infection;
but by fourth or fifth
day, "red strawberry
Rapid strep test,
wound or throat
Staphylococcus aureus Diffuse "sunburn" rash
that desquamates over 1
to 2 weeks
All ages, but
most common in
involvement of three
or more organ
systems; about 50
percent of cases
women around onset
patients at increased
risk; condition out of
proportion to wound
Kawasaki's disease Idiopathic Erythematous rash on
hands and feet;
scarlatiniform rash on
trunk and perineum;
than 8 years of
age, with peak
incidence at 1
often than girls
Winter and spring;
high fevers, cervical
involvement; can be
abnormalities in 20
to 25 percent of
Chickenpox Varicella-zoster virus Initially, papules, which
evolve into vesicles
("dewdrops on a rose
petal") and eventually
into pustules and crusts;
rash beginning on face
and spreading inferiorly
to trunk and extremities
90 percent of
cases in children
less than 10
years of age; 5
percent of cases
in persons older
than 15 years
of headache, general
aches, backache and
malaise is typically
absent in children;
may have all forms
of lesions at the
same time; vesicles
evolving to shallow
erosions common on
of palate; may also
have vesicles on
and genital mucosa
Varicella-zoster virus Begins as erythematous
rapidly evolves to
All ages, but
Prodrome of unusual
with lesions rarely
pain often severe;
more common in
thoracic and facial
Rickettsialpox Rickettsia akari Generalized
involvement of mucous
involvement of palms or
All ages; urban
mice to humans via
mites; formation of
papules 7 to 10 days
after initial bite;
of a black eschar
over healing lesion;
occurring 3 to 7 days
after initial lesion
and lasting up to a
usually mild course
Erythema nodosum Various causes (see Table 4) Bright-red nodules (3 to
20 cm in diameter)
scattered bilaterally but
not symmetric; most
frequently on lower legs
young adults 15
to 30 years of
but also found on knees
and arms; rarely found
on face and neck; lesions
often tender and
often than males culture for group A
radiograph to rule
in 50 percent of
cases; fever and
Adapted with permission from Kaye ET, Kaye KM. Fever and rash. In: Fauci AS, et al., eds. Harrison's Principles of internal medicine.
14th ed. New York: McGraw-Hill, Health Professions Division, 1998:90-7, with additional information from Fitzpatrick TB, et al. Color
atlas and synopsis of clinical dermatology: common and serious diseases. 3d ed. New York: McGraw-Hill, Health Professions Division,
Maculopapular eruptions are most frequently seen in viral illnesses (Figure 1) and immune-mediated syndromes. These
eruptions can have many causes, including drug reactions and bacterial infections. Infectious exanthems are common and
are defined as generalized cutaneous eruptions associated with a systemic infection. It is helpful to consider centrally and
peripherally distributed eruptions separately because each type has its own differential diagnosis.2
Centrally Distributed Eruptions
Centrally distributed maculopapular eruptions are more common than peripheral eruptions.2These eruptions include
rashes that begin centrally, first affecting the head and neck, and then progress peripherally.
Viral Exanthems. Viral etiologies of rashes include rubeola, rubella, erythema infectiosum and roseola.4
The exanthem of rubeola begins around the fourth febrile day, with discrete lesions that become confluent as they spread
from the hairline downward, sparing the palms and soles. The exanthem typically lasts four to six days. The lesions fade
gradually in order of appearance, leaving a residual yellow-tan coloration or faint desquamation. Rubeola is also
distinguished by the presence of Koplik's spots in the oral mucosa.1,2
Rubella is similar to rubeola. However, it causes less severe symptoms, and its exanthem characteristically has a shorter
duration (two to three days).1,2
FIGURE 1. Maculopapular rash in a
nonspecific viral exanthem.
FIGURE 2. Maculopapular rash of
erythema infectiosum (fifth disease).
Erythema infectiosum, or fifth disease, is caused by human parvovirus B19. This disease primarily affects children
between three and 12 years of age, although it can present as a rheumatic syndrome in adults. The prodrome may consist
of fever, anorexia, sore throat and abdominal pain. Once the fever resolves, the classic bright-red facial rash ("slapped
cheek") appears. Within several days, the exanthem progresses to a diffuse, lacy, reticular rash that may wax and wane for
six to eight weeks (Figure 2). Human parvovirus B19 infection is of particular concern in pregnant women because it has
been associated with fetal hydrops and subsequent fetal death.1,4,7,8
Roseola, or exanthema subitum, is caused by human herpesvirus 6. This
disease occurs in children less than three years of age. As in fifth disease,
the rash appears after the resolution of several days of high fever. The
diffuse maculopapular eruption often spares the face and is of short
duration, typically fading within three days.7,8
Lyme Disease and Erythema Migrans. Lyme disease is the most
commonly reported vector-borne illness in the United States.7 It is caused by the spirochete Borrelia burgdorferi, which is
transmitted by the bite of a tick (Ixodes species). Endemic areas in the United States include the northeastern,
mid-Atlantic, north-central and far-western regions.9
Erythema migrans, the pathognomonic rash, develops in about 80 percent of
patients with Lyme disease.6This enlarging, erythematous macular rash begins as
a macule or papule at the site of inoculation (Figure 3). Systemic symptoms,
including fever, chills, myalgias, headaches and arthralgias, often accompany the
The rash is more common on the proximal extremities, in body creases and on the
chest. It enlarges over a period of days to weeks, reaching a maximum diameter of
3 to 68 cm (median diameter: 15 cm).1,10
Roseola is caused by human herpesvirus 6 and
usually occurs in children less than three years
of age. A diffuse maculopapular eruption
appears after the resolution of high fever; the
face is usually spared.
FIGURE 3. Erythema migrans on upper
arm in Lyme disease.
The primary lesion may show central clearing, central necrosis, induration or vesiculation. Smaller secondary lesions may
develop in up to 20 percent of patients with Lyme disease and may
indicate early hematogenous spread.10
Borrelia lymphocytoma is a painless bluish-red nodule or plaque that
may develop in early Lyme disease. The lesion is usually located on the
earlobe, nipple or scrotum.9
Complications of untreated Lyme disease include carditis,
neuroborreliosis, arthritis and acrodermatitis chronica atrophicans.9
Drug-Related Eruptions. Drug reactions can present as any dermatologic morphology and show no predilection for age,
gender or race. Exanthematous eruptions most commonly occur in association with the administration of penicillins or
cephalosporins. The rash usually appears within the first week after the offending drug is started and typically resolves
within days after the drug is discontinued. Drug-related reactions can be difficult to distinguish from viral exanthems, but
they may be more intensely erythematous and pruritic.1,2,11
Erythema Multiforme. The most common peripheral eruptive maculopapular rash, erythema multiforme occurs more
frequently in men than in women and most often affects persons between 20 and 30 years of age. The rash, which can be
recurrent, shows a predilection for palms, soles, knees and elbows. Although erythema multiforme has a number of
known etiologies (Table 3),1,4,6 it is idiopathic in more than 50 percent of affected patients.1,6
Etiologies of Erythema Multiforme
Idiopathic (more than 50 percent of cases)
Herpes simplex virus
Borrelia lymphocytoma is a painless bluish-red
nodule that may be seen in early Lyme disease.
The lesion is usually located on the earlobe,
nipple or scrotum.
Information from Fitzpatrick TB, et al. Color atlas and synopsis of clinical dermatology: common and serious diseases. 3d
ed. New York: McGraw-Hill, Health Professions Division, 1997; Weber DI, Cohen MS, Fine JD. The acutely ill patient with
fever and rash. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and practice of
infectious diseases. 5th ed. Philadelphia: Churchill Livingstone, 1999:633-50; and Habif TP. Clinical dermatology: a color
guide to diagnosis and therapy. 3d ed. St. Louis: Mosby, 1996.
Erythema multiforme begins as a macular eruption (Figure 4). The dull-red lesions advance from macules to papules, with
prominence of characteristic target-shaped lesions. Vesicles and bullae may develop in the center of the papules. In many
patients, the mucous membranes of the mouth and lips are involved.1
The illness is classified as minor or major, depending on severity. In erythema
multiforme minor, bullae and systemic symptoms are absent. The eruption is
typically confined to the extensor surfaces of extremities and only rarely involves
the mucous membranes. Recurrent episodes of erythema multiforme minor
usually precede an outbreak of herpes simplex by several
days. [corrected]Recurrences may be prevented with chronic acyclovir (Zovirax)
Erythema multiforme major most often results from a drug reaction. Mucous
membranes are always involved. The eruption tends to become bullous and
systemic symptoms, including fever and prostration, are present. Eating may be complicated by cheilitis and stomatitis,
and micturition may be difficult because of balanitis and vulvitis. Conjunctivitis may be severe and can lead to keratitis
and ulceration. Lesions may also be found in the pharynx, larynx and trachea. Rarely, erythema multiforme major can be
life-threatening and can progress to necrotizing tracheobronchitis, meningitis, blindness, sepsis and renal tubular
Secondary Syphilis. The rash of secondary syphilis can be diffuse, with localized eruptions often occurring on the head,
neck, palms and soles. The lesions are typically brownish-red or pink macules and papules, but they may be
papulosquamous, pustular or acneiform. The eruption usually occurs two to six months after the primary infection and
two to 10 weeks after the primary chancre.12
Patients often present with acute constitutional symptoms, and asymptomatic flat-topped macules and papules (mucous
patches) are commonly found on the oral and genital mucosa. Classic condyloma lata may also be found in the
Others. Meningococcemia, Rocky Mountain spotted fever and dengue fever--all potentially life-threatening
infections--may initially present with erythematous maculopapular lesions before advancing to a petechial exanthem.3,13
FIGURE 4. Erythema multiforme
associated with sulfa drug
Petechial rashes warrant immediate evaluation to rule out severe,
life-threatening illness. For proper assessment of an acutely ill patient
with a petechial rash, the physician must be familiar with the common
infectious and noninfectious etiologies. Prompt, accurate diagnosis and
early treatment can be life-saving in patients with meningococcemia,
rickettsial infections and bacteremia.3,13
Meningococcal infections are a worldwide concern. These infections occur sporadically or in epidemics, most commonly
in the midwinter months.1 Seeding of Neisseria meningitidisfrom the nasopharynx may result in acute meningococcal
septicemia, meningococcal meningitis or chronic meningococcemia. The risk of meningococcal disease is highest in
infants, asplenic patients, alcoholics and patients with a complement deficiency
(especially C5 to C8).1
In some patients, the typical prodrome of cough, headache, sore throat, nausea
and vomiting may be of short duration. Patients with acute meningococcemia
appear ill and usually present with a characteristic petechial rash (Figure 5), a
high, spiking fever, tachypnea, tachycardia and mild hypotension. In the early
stages of disease, the rash may be maculopapular.14 Signs and symptoms of
meningeal irritation may be helpful, given that up to 88 percent1 of patients with
meningococcemia develop meningitis.1,13-15
Chronic meningococcemia is a rare condition. Patients may present with
intermittent rash, fever, arthritis and arthralgias occurring over a period of weeks to several months. In some patients,
the chronic form advances to acute meningococcemia.1 The rash may be polymorphous, with maculopapular lesions
usually located around a painful joint or pressure point, nodules on the lower extremities and petechiae of variable
Rocky Mountain Spotted Fever
Rocky Mountain spotted fever is the most common rickettsial disease in the United States.16It is caused by Rickettsia
rickettsii, which is transmitted through a tick bite or contact with tick feces or tissue juices.1
The disease occurs most often in young men between April and September.16 In the United States, the areas with the
highest prevalence of Rocky Mountain spotted fever are Oklahoma and the southern Atlantic states.6
The prodrome may include malaise, chills, a feverish feeling, anorexia and irritability. The onset of symptoms may be
abrupt, with the predominant features being fever (94 percent), severe headache (86 percent), generalized myalgia (83
percent), shaking rigor, photophobia, prostration and nausea. The diagnosis can be difficult when the onset is gradual and
no rash is present, as is the case in up to 20 percent of adults and 5 percent of children with Rocky Mountain spotted
Petechial rashes warrant immediate evaluation
to rule out severe, life-threatening illness.
FIGURE 5. Petechiae in
When rash is present, it develops on approximately the fourth day of
illness. Its appearance, combined with the temporal evolution, is
characteristic of Rocky Mountain spotted fever. The rash typically
begins as pink macules, 2 to 6 mm in diameter, located on the wrists,
forearms, ankles, palms and soles. Within six to 18 hours, the rash
spreads centrally to involve the arms, thighs, trunk and face. In the
ensuing one to three days, the lesions evolve into deep-red papules.
Within two to four days after onset of the rash, the lesions become
Viral illnesses known to cause petechial rashes include coxsackievirus A9, echovirus 9, Epstein-Barr virus and
cytomegalovirus infections, atypical measles and viral hemorrhagic fevers caused by arboviruses and arenaviruses.
Coxsackievirus and echovirus infections in children can produce severe illness and, at times, are difficult to distinguish
Included in the differential diagnosis of petechial rash are disseminated gonococcal infections, bacteremia,
staphylococcemia and thrombotic thrombocytopenic purpura.
Diffuse Erythema with Desquamation
Scarlet fever provides the classic example of an erythematous rash with subsequent desquamation. Most common
between one and 10 years of age,18 scarlet fever usually follows an acute infection of the tonsils or skin by group A
beta-hemolytic streptococci that produce an erythrogenic exotoxin.2 Patients may appear acutely ill and have fever, sore
throat, headache, chills, nausea and vomiting.1,18
The rash begins as finely punctate erythema on the superior trunk and face two to three days after the onset of illness.
The erythema quickly spreads to the extremities. When present, petechiae in the antecubital and axillary skin folds
(Pastia's lines) can be helpful in making the diagnosis.1,2
Initially, the tongue may appear white, with red, swollen papillae (white strawberry tongue), but by the fourth or fifth
day, it becomes bright red (red strawberry tongue). The oral mucosa may have punctate erythema or petechiae, and the
tonsils may be acutely infected.1
The exanthem varies in intensity. However, it usually fades in four to five days and is followed by diffuse desquamation.1
The infection may be mild, and patients may present with only complaints of desquamation. Rarely, the streptococcal
infection may produce a toxic-shocklike picture that results in hypotension and multisystem failure. Many of these
The rash of Rocky Mountain spotted fever
develops on about the fourth day of illness as
small macules located on the wrists and ankles.
The lesions progress to papules and then to
patients have a localized tissue infection that progresses to necrotizing fasciitis, which usually warrants immediate
Toxic Shock Syndrome and Scalded Skin Syndrome
Staphylococcus aureus is the organism responsible for classic toxic
shock syndrome and scalded skin syndrome. Toxic shock
syndrome can present with hypotension, erythema, fever and
multisystem dysfunction.3Most cases of nonmenstrual toxic shock
syndrome occur in the postoperative setting.1
Several different staphylococcal exotoxins have been implicated.
The syndrome may result from infection, or it may occur because
of simple colonization with S. aureus.3 Staphylococcal scalded skin
syndrome occurs in infants, young children and adults with
immunosuppression or renal impairment.1
The rash is usually diffuse and can present as bullous impetigo, scarlatiniform lesions or diffuse erythema (Figure 6). The
mucous membranes are spared in most patients. During the physical examination, the physician should attempt to elicit
Nikolsky's sign (shearing of the skin with gentle lateral pressure).1,3,4
Kawasaki's disease, or mucocutaneous lymph node syndrome, is an acute febrile illness that affects infants and young
children (mean age: 2.6 years). The disease is uncommon after the age of 12 years.6
In patients with Kawasaki's disease, fever begins abruptly, and the temperature is typically higher than 40°C (104°F). The
fever lasts five to 30 days (mean duration: 8.5 days) and does not respond to antibiotics and antipyretics.6,8
FIGURE 6. Diffuse erythema in toxic shock syndrome.
The rash appears within three days of the onset of fever and can
vary in character. Frequently, the rash is scarlatiniform on the
trunk and erythematous on the palms and soles, with subsequent
distal desquamation. Mucous membrane involvement is common
and includes hyperemic bulbar conjunctiva, injected oropharynx,
dry, cracked lips and a strawberry tongue.1,6
The physical examination may reveal nonsuppurative cervical
lymphadenopathy (more than 1.5 cm in diameter). Coronary
artery abnormalities develop in 20 to 25 percent of patients with
Kawasaki's disease.19Cardiovascular complications are the major
cause of short-term and long-term morbidity and mortality.1,6,8,19
Ehrlichiosis, a rickettsial-like infection, can occasionally be
associated with a clinical picture similar to toxic shock syndrome,
including diffuse erythema. Streptococcus viridans bacteremia is
another rare cause of generalized erythema. Finally, enteroviral
infections, toxic epidermal necrolysis, graft-versus-host reaction,
erythroderma and generalized pustular psoriasis (von
Zumbusch's psoriasis) may present with diffuse erythema.1,3
Varicella-Zoster Virus Infections
Varicella-zoster virus is the most infectious of the human
herpesviruses. It is responsible for varicella (chickenpox) and
herpes zoster (shingles).20
Varicella. Primary infection with varicella-zoster virus results in
chickenpox, a common childhood illness. Its highest incidence is in late winter and spring.2 The disease is typically more
severe in adults and immunocompromised patients.1,6
Etiologies of Erythema Nodosum
Idiopathic (40 percent of cases)
Hepatitis C virus
Systemic lupus erythematosus
Information from Fitzpatrick TB, et al. Color atlas and
synopsis of clinical dermatology: common and
serious diseases. 3d ed. New York: McGraw-Hill,
Health Professions Division, 1997, and Weber DI,
Cohen MS, Fine JD. The acutely ill patient with fever
and rash. In: Mandell GL, Bennett JE, Dolin R, eds.
Mandell, Douglas, and Bennett's Principles and
practice of infectious diseases. 5th ed. Philadelphia:
Churchill Livingstone, 1999:633-50.
The clinical presentation consists of rash, fever and general
malaise.2 A mild prodrome lasting one to two days before
appearance of the rash is not uncommon. The rash typically begins
on the face, scalp or trunk and then spreads to the extremities.8
The lesions appear as erythematous macules and progress to
papules with an edematous base (Figure 7). The papules quickly
evolve into vesicles, with each vesicle initially having the
appearance of "a dewdrop on a rose petal."1 The vesicles evolve
into pustules, which become umbilicated and subsequently crust
over in the ensuing eight to 12 hours. An enanthema may be noted,
and vesicles may evolve to shallow erosions, primarily on the palate. On physical examination, lesions in all stages may be
Complications are unusual in immunocompetent patients. In children, the most common complication is secondary
bacterial infection of excoriated lesions.7
The central nervous system (CNS) is the most common site of extracutaneous involvement in children. Cerebellar ataxia is
the most frequently encountered syndrome. Other possible CNS complications include encephalitis, meningitis,
transverse myelitis and, rarely, Reye's syndrome (especially subsequent to aspirin use). Varicella pneumonia and
encephalitis can be serious complications in adults. Additional rare complications in children and adults include
myocarditis, corneal lesions, nephritis, arthritis, bleeding diatheses,
acute glomerulonephritis and hepatitis.1,2,7,21
Herpes Zoster. After the primary infection, the varicella-zoster virus lies
dormant in the dorsal root ganglia. Herpes zoster is caused by
reactivation of the virus.20 Although shingles can occur at any age, its
incidence increases significantly with age and in immunocompromised
patients. An estimated 10 to 20 percent of the general U.S. population
will have herpes zoster at some time in life.20
The characteristic vesicular rash of herpes zoster usually affects a single dermatome and rarely crosses the
midline (Figure 8). The most common locations are the chest (approximately 50 percent of cases) and the face
(approximately 20 percent of cases).20 A prodrome of unusual skin sensations may evolve into pain, burning and
paresthesias, which precede the rash by two to three days.
FIGURE 7. Rash of varicella (chickenpox).
The most common location for herpes zoster is
the chest, followed by the face. Only a single
dermatome is usually affected, and the lesions
rarely cross the midline.
The rash begins as an erythematous maculopapular eruption that rapidly evolves
to a vesicular rash.21 In about 5 percent of patients, the rash may be accompanied
by headache, malaise and fever.1Drying of the lesions with crust formation
generally occurs in seven to 10 days, and the lesions usually resolve in 14 to 21
Pain is the most debilitating feature of herpes zoster, and postherpetic neuralgia
is the most common long-term complication. Postherpetic neuralgia is uncommon
in young patients but may affect as many as 50 percent of patients more than 50
years of age.21
Other potential complications of herpes zoster include secondary infection,
meningoencephalitis, transverse myelitis, pneumonitis, hepatitis, myocarditis,
pancreatitis, esophagitis, cystitis, granulomatous arteritis, conjunctivitis and
Ramsay Hunt syndrome (herpes zoster involving the facial and auditory nerves). When herpes zoster affects the eye
(herpes zoster ophthalmicus), an ophthalmologist should always be consulted.1,20,21
Staphylococcal bacteremia may present with a widespread pustular eruption. Gonococcemia may also produce a pustular
rash, although other lesion types, such as macules, petechiae and papules, are usually present.3
In immunocompromised patients, disseminated herpes simplex virus infection must be considered. Patients with
underlying liver disease, renal dysfunction or diabetes are particularly susceptible to infection with Vibrio
vulnificus, which is acquired from eating seafood, exposure to sea water or injury when handling crabs. Rickettsia
akari,transmitted by a house mite, is the cause of rickettsialpox, a mild disease characterized by a local eschar, a
papulovesicular rash and a mild clinical course.1-4,12
Erythema nodosum is an acute inflammatory and immunologic
process involving the panniculus adiposus (the fatty tissue layer
underlying the skin).1 A number of etiologies have been
identified(Table 4).1,4 This condition is more common in women than
Presenting features often include fever, malaise and arthralgias. The
characteristic nodules are painful and tender. The lesions most often
develop on the lower legs, knees and arms (Figure 9). The course of
erythema nodosum depends on the specific cause, but spontaneous resolution can be expected within six weeks.1,2
FIGURE 8. Dermatomal distribution of
rash in herpes zoster.
FIGURE 8. Erythema nodosum.