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23/11/2008
This Book is not published by eMedicine .It is just a selection of cases from eMedicine website by Ali Faris Haider.
Preface
Since the best way of learning medicine is to study medical problems I collected some of the common cases from eMedicine website and put them in this book without editing the contents so that everyone can enjoy solving these Medical problems. What is eMedicine? eMedicine: It is web-based and consists of clinical overviews of disease entities by experts in the field. Continuously updated, mainly for professionals, over 10 000 physician authors on 7000 diseases, Articles undergoes 4 levels of physician peer review plus an addi onal review by a Pharmacy editor prior to publication, 30 000 mul media les % of radiology residents use it as ,12 the first source of information. eMedicine is read by doctors and medical students from approximately 120 countries. eMedicine(www.emedicine.com) sends a weekly case via email to its subscribers. This book is dedicated to Junior and senior doctors. If you find this book useful; please remember me in your prayer. Dr. Ali Faris Haider 13-12-2008
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On his arrival to the emergency department, the patient continued to have the sensation that his heart was racing. He denies having any chest pain, nausea, vomiting, diaphoresis, light-headedness, or recent illness. He felt well before this episode. He denies having any symptoms of infection, such as fever, cough, vomiting, diarrhea, anorexia, or dysuria. He reports increased stress at work and is drinking as many as 4 cups of coee a day. He reports no notable history of medical conditions except for a similar episode of a rapid heart rate about 4 years ago; for this, he was treated with an unknown drug for 2 years. His family history is signicant for a father who died of a myocardial infarc on at 45 years of age. The pa ent takes 1 baby aspirin daily. He denies using any over-the-counter or illicit drugs; however, he smokes 3 packs of cigare es per week. On physical examina on, the pa ent is afebrile and has a heart rate of 165 bpm and a blood pressure of 138/79 mm Hg. He appears well and is in no acute distress. Findings on head and neck examination are unremarkable. He has no jugular venous disten on. His heart rate is rapid and irregular, with an audible S1 and S2 and no gallops, rubs, or murmurs. His lungs are clear bilaterally. His abdomen is soft, nontender, and without any
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What is the diagnosis? Hint: Paramedics gave the patient a single dose of adenosine, which had no lasting effect on the rapid rhythm. o Ventricular fibrillation o Atrial fibrillation o Torsade de pointes o Sinus tachycardia
Diagnosis: Atrial fibrillation (AF) with a rapid ventricular response. : Discussion: The ECG shows an irregular heart rhythm with no discernible P waves. Rapid atrial fibrillation (AF) may be hard to differentiate from a narrow supraventricular tachycardia (SVT) without close examination of an ECG. The two conditions can result in similar symptoms of heart palpitations and shortness of breath. Patients with rapid AF palpitations are not uncommonly given adenosine to treat presumed SVT, as in this case. Although this treatment is typically unsuccessful, the underlying atrial rhythm may be accurately determined when the heart rate briefly slows. The conversion from a normal sinus rhythm to AF may be due to a number of conditions, including hyperthyroidism, anemia, infection, ischemic heart disease, valvular disease, drug intoxication, or use of stimulants. Increased stress and overconsumption of coffee are likely to have been the instigating factors in this overconsumption patient. AF is a common arrhythmia characterized by chaotic atrial depolarizations without effective atrial contractions. This rhythm is often seen with increasing age, with a male predominance. This arrhythmia can result in male decreased cardiac output and the formation of atrial thrombi. Many patients with AF are asymptomatic, and most have recurrent episodes without knowledge of them. The American College of Cardiology established a classification system for AF that is based on its duration and etiology. The categories are paroxysmal AF, persistent AF, permanent AF, and lone AF. In paroxysmal AF, the episodes last less than 1 week. If they recur, the condi on is considered recurren paroxysmal AF. In persistent t AF, the episodes last longer than 1 week. In permanent AF, the episode lasts longer than 1 year without any attempts for conversion or with attempts that fail. Finally, in lone AF, no underlying structural cardiac or pulmonary disease is found. Patients with lone AF have a low risk of mortality and thromboembolism and may y have paroxysmal, persistent, or permanent AF. The workup for AF involves careful history taking and physical examination, laboratory studies (including a CBC CBC, serum electrolyte tests, toxicology screening, and thyroid function tests), ECG, chest radiography, and echocardiography. The patient's history should include the time of onset, the frequency of episodes, any associated symptoms, and any history of treatment for AF. Laboratory studies may be useful in determining possible etiologies of AF. The ment WBC count may help in finding an underlying infection, and the hemoglobin concentration may demonstrate anemia. Electrolyte levels, such as magnesium and potassium levels, may be abnormal, and an elevated creatinine value may indicate a renal insufficiency. Certain illicit drugs can cause a rapid heart rate; therefore, a toxicology screening may be useful when indicated. Hyperthyroidism can predispose patients to AF. For this reason, an evaluation of thyroid function with measurement of the patient's thyroid thyroid-stimulating hormone (TSH) level is warranted. AF can be diagnosed when the ECG shows an irregular rhythm with the absence of P waves. In addition, examine the patient for any signs of left ventricular hypertrophy, bundle branch blocks, and atrioventricular ient
Figure 1
Hint The pa ent looks comfortable despite changes on his ECG. He had symptoms of a common cold 3 weeks ago.
Figure 1
For the rst 2 days of this illness, the pa ent had a mild runny nose, a sore throat, and some diarrhea, all of which were self-limited. Since his illness began, he has had an on-and-off headache, in addition to increasing weakness and anorexia. On systemic review, the findings are otherwise essentially negative, including the
Figure 1
On physical examination, the patient is afebrile, with a blood pressure of 125/67 mm Hg, a pulse of 75 bpm, a respiratory rate of 20 breaths/min, and an oxygen satura on of 91% while breathing room air. The pa ent appears younger than his stated age. He is in no acute distress. The neck examination shows no appreciable jugular venous distension or carotid bruits. His heart sounds are remarkable for a regular heart rhythm, with frequent skipped beats and a slightly accentuated second heart sound. No murmurs, rubs, or gallops are appreciated. Auscultation of his chest reveals distant breath sounds with no wheezing, crackles, or rhonchi. There is no peripheral edema of the lower extremities. The remainder of the physical examination is unremarkable. A panel of preoperative blood tests and an electrocardiogram (ECG) are ordered. While the patient is waiting in the preoperative holding area, he experiences an episode of lightheadedness. Upon noting a rapid pulse, a technician attaches leads to obtain a cardiac rhythm strip and an ECG. His blood pressure is recorded at 80/46 mm Hg. A 12-lead ECG is obtained (see Figure 1).
Diagnosis: Nonsustained ventricular tachycardia Discussion: A wide-complex tachycardia is a cardiac dysrhythmia with a ventricular rate that exceeds 100 bpm in the se ng complex of a QRS dura on greater than or equal to 120 milliseconds. A widecomplex tachycardia can originate from either a ventricular focus or a supraventricular focus associated with a conduction abnor abnormality. In this case, based on the QRS morphology (the QRS width being greater than 140 milliseconds at the widest leads) and the atrioventricular dissociation (see arrows), the ECG was determined to have the characteristics of ventricular tachycardia (see subsequent discussion on how to determine the focus of a wide complex tachycardia). wide-complex
Figure 1
Ventricular tachycardia is the most common cause of wide complex tachycardias, accounting for as many as wide-complex 80% of cases. The frequency can be even higher in pa ents with structural or ischemic heart disease. Ventricular tachycardia also occurs in patients with electrolyte abnormalities, such as hypokalemia and hypomagnesemia, as well as in hypoxemic patients, individuals with acidemia, and patients with mitral va valve prolapse. The rhythm can occasionally occur in individuals without any identifiable risk factors. Adverse drug reactions can also induce ventricular tachycardia by prolonging the QT interval. Drugs that are known to
As mentioned above, the patient in this case was diagnosed with ventricular tachycardia, and his elective surgery for repairing the hernia was put on hold. An electrophysiology study was arranged after consultation with a cardiologist. An arrhythmogenic focus of myocardial irritability, which was thought to be caused by scar tissue from an unrecognized previous myocardial infarction, was identified during the study. The patient had an automatic internal cardiac defibrillator placed and, subsequently, his hernia was successfully repaired.
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The pa ent is urgently placed on a cardiac monitor, and an 18guage peripheral intravenous (IV) line is inserted into the antecubital fossa, through which infusion of normal saline is ini ated. The pa ent is given 2 doses of IV hydromorphone, without significant improvement in his pain or abdominal tenderness. An upright, portable anterior/posterior chest radiograph is obtained, and it is noted to appear normal, with no air visualized under the diaphragm. An abdominal ultrasonogram is taken that shows no evidence of gallstones or biliary wall
What is the cause of the patient's acute abdominal pain? Hint: The acute event is likely the result of an underlying pathology. o o o o Gastroesophageal reflux disease Acalculous cholecystitis Acute pancreatitis Perforated peptic ulcer
Diagnosis: Perforated peptic ulcer Discussion: Transverse cuts obtained from the CT scan of the abdomen and pelvis (see Figures 1 and 2) showed free air underneath the diaphragm consistent with a perforated viscous. The images also demonstrated fluid in the region of the distal antrum/pylorus, with a small pocket of air in this fluid, suggesting that the stomach was the site of the perforation. The patient's history of alcohol use pointed to a diagnosis of a perforated gastric ulcer. 's Regarding a potential differential diagnosis in epigastric abdominal pain, several life life-threatening etiologies that must be recognized and treated urgently are possible. Cardiovascular etiologies, including acute coronary Cardiovascular syndrome and aortic dissection, must be considered, even when frank chest pain is absent. Numerous gastrointestinal causes can present in a very similar fashion. Most commonly, a relatively benign cause, such a as mild esophagitis and gastritis, is responsible. The pain of an uncomplicated peptic ulcer is comparable to that of a perforated peptic ulcer, although it is typically chronic in nature. Gallbladder disease ranges from relatively mild biliary colic to acute cholecystitis. Liver diseases include acute hepatitis; masses, such as abscesses or te tumors; gonococcal or chlamydial perihepatitis (Fitz (Fitz-Hugh-Curtis syndrome) in women; and acute cholangitis. Curtis Acute pancreatitis may be present, with or without the presence of gallbladder disease. Acute appendicitis may presence first present with upper abdominal or midabdominal pain before localizing to the right lower quadrant. Pulmonary processes, such as pneumonia, must also be considered in patients complaining of upper abdomi abdominal pain, even in the absence of cough or shortness of breath. With such a broad differential diagnosis in the presentation of epigastric abdominal pain, the workup (including laboratory investigations and radiologic imaging) has to be individualized based on age and other risk factors for each potential disease process and on the characteristics and associated symptoms of the pain. Additionally, repeat assessment of the symptoms and physical examination should be performed during the course of the evaluation. The administration of parenteral pain medication will often enable localization of the source of pain on. and assessment of the severity of the disease; pain medication should not be withheld for fear of "masking" a potentially serious disease process. As illustrated in this case, the patient had a somewhat vague examination with an essentially normal initial workup, including no evidence of perforation on an upright radiograph at presentation; this may have been dismissed as "benign" pain if it were not for the persistence of pain and for tenderness despite the administration of pain medication. Uncomplicated peptic ulcer disease (PUD) is highly prevalent in the United States. When combined with duodenal ulcers, the incidence is 1.8%, or approximately 500,000 new cases annually. Additionally, there are new about 4 million recurrences yearly. Approximately 90% of duodenal ulcers and 75% of gastric ulcers are associated with Helicobacter pylori infection. Although it is still unclear, H. pylori appears to cause injury to the stomach and duodenum through 3 poten al mechanisms, including the produc on of toxins that cause local tissue injury, the induction of a mucosal immune response, and the increase of gastrin levels with an increase in acid secretion. After H. pylori infection, NSAIDs are the most common cause of PUD. The risk of disease and ri complications (such as hemorrhage or perforation) are proportional to the daily dose taken. Advanced age and concurrent use of anticoagulants or steroids also increase the risk for complication. Other factors that may predispose a patient to gastric ulceration include chronic alcohol intake, smoking, and infection.
Figure 1
Hint The pa ent also complains of chest pressure. His blood pressure is 80 mm Hg systolic, 50 mm Hg diastolic.
Figure 1
On physical examina on, the pa ent has an elevated temperature of 101.3F (38.5C), a blood pressure of 130/76 mm Hg, a pulse of 110 bpm, and a respiratory rate of 20 breaths/min. The pa ent is not in acute distress, but he is mildly ill-appearing and diaphoretic. His oropharynx is clear, with slightly dry mucous appearing diaphoretic. membranes. His lungs are clear to auscultation, and his heart rate is regular, without murmurs. The abdominal
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What is the diagnosis? Hint: This is the most common acute condition related to the sigmoid colon. o o o o Acute diverticulitis Colon cancer Acute bacterial peritonitis Acute appendicitis
Diagnosis: Acute diverticulitis Discussion: Acute diverticulitis results from inflammation of a diverticulum (small mucosal and submucosal herniations through the circular muscle layer of the colonic wall) secondary to fecal obstruction. The obstruction typically obstruction. occurs at the neck of the diverticulum; solidified stool, which typically forms a fecalith, abrades the mucosa within or at the neck of the diverticulum. In uncomplicated cases (typically characterized by a well well-appearing patient without peritonitis and systemic signs/symptoms), the inflammatory process is confined to the colonic atient wall; however, the obstruction, with subsequent high intraluminal pressure within the diverticula, can lead to a microperforation which, in turn, allows translocation of bacteria through the colonic wall, pericolic abscess llows forma on, and diuse peritoni s. Only 4% of pa ents diagnosed with diver culi s are younger than 40 years -4% 2 old; the condition is predominantly found in elderly populations.
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s.
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What is the patient's condition as verified by the MRI? Hint: Look closely at the cauda equina on the MRI images. o o o o Spinal epidural abscess Guillain-Barr syndrome Transverse myelitis Multiple sclerosis
Diagnosis: Guillain-Barr syndrome Barr Discussion: The lumbrosacral MRIs (see Figures 1 and 2) demonstrate nerve root enhancement of the cauda equina on axial post-contrast T1-weighted sequences. The localization of progressive weakness includes spinal cord lesions weighted (such as transverse myelitis or anterior spinal artery syndrome), peripheral neuropathies (such as those caused peripheral by heavy metals), neuromuscular junction diseases (such as that caused by organophosphate pesticides), myasthenia gravis, botulism, and myopathies (such as dermatomyositis). The presence of progressive ascending weakness, areflexia, autonomic dysfunction, elevated CSF protein without pleocytosis, and enhancement of the cauda equina nerve roots on lumbrosacral MRIs make the diagnosis of Guillain Barr syndrome most probable Guillain-Barr in this patient.
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Guillain-Barr syndrome is an acute, idiopathic, monophasic, acquired inflammatory demyelinating polyradiculoneuropathy (AIDP) that affects both children and adults. It is a heterogeneous syndrome, with several variant forms. AIDP is the prototype of Guillain-Barr syndrome, and it is the most common form in North America, Europe, and most of the developed world (where it accounts for about 85-90% of cases). Guillain-Barr syndrome can occur at any age, but there appears to be a bimodal distribution, with peaks in young adulthood (15-35 y) and in the elderly (50-75 y). The cause of Guillain-Barr syndrome is unknown, but the disorder is thought to result from a postinfectious immune-mediated process called molecular mimicry that predominantly damages the myelin sheath of peripheral nerves. Approximately two thirds of patients report a history of an antecedent respiratory tract or gastrointes nal infec on 2 weeks before the onset of neurologic -4 symptoms. A variety of infectious agents have been associated with Guillain-Barr syndrome, although Campylobacter is the most frequent. Other organisms that commonly precede Guillain-Barr syndrome include cytomegalovirus, Epstein-Barr virus, Haemophilus influenzae, Mycoplasma pneumoniae, the enterovirus family, hepatitis A and B, herpes simplex virus, and Chlamydophila (formerly Chlamydia) pneumoniae. The typical presentation of Guillain-Barr syndrome is fine paresthesias in the toes and fingertips, followed by symmetric lower-extremity weakness that may ascend, over hours to days, to involve the arms and the muscles of respiration. Pain, predominately back, lower-limb and abdominal pain, is often a prominent feature of the syndrome. The physical examination reveals symmetric weakness, with diminished or absent reflexes and variable loss of sensation in a stocking-glove distribu on. Signs of autonomic dysfunc on are present in 50% of patients, and they include cardiac dysrhythmias, orthostatic hypotension, transient or persistent hypertension, ileus, constipation, and bladder dysfunction. Deviation from the classic presentation of ascending progression of
Figure 1
What is the diagnosis? Hint: The ECG results suggest a chronic condition. o Pulmonary embolus o Chronic obstructive pulmonary disease o Acute bacterial pneumonia o Stable angina
Diagnosis: Chronic obstructive pulmonary disease Discussion: The ECG demonstrates a constellation of findings that suggest COPD, including sinus tachycardia, a rightward axis, P pulmonale (a P wave amplitude > 2.5mV in the inferior leads), a low QRS voltage, and a right bundle branch block (RBBB). In addition, the slight ST segment depressions in the inferior leads are suggestive of prominent atrial depressions repolarization abnormalities and are seen in COPD COPD.
Figure 1
Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of death in the United States. COPD is defined as a disease state characterized by airflow obstruction caused by chronic bronchitis or emphysema. The airflow obstruction generally is progressive, and it may be accompanied by partially reversible airway hyperreactivity. The condition was rst described in Western Europe in the early 19th century by Badham (1808) and Laennec (1827), who made the classic descrip on of chronic bronchi s and emphysema. A Bri sh medical textbook of the 1860s described the familiar clinical picture of chron bronchitis as an advanced ic disease, with repeated bronchial infections, that ended in right heart failure. The modern definition of chronic bronchitis and emphysema which incorporated the concept of airflow obstruction was proposed by participants of the Ciba symposium of 1958.
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A second large-bore peripheral intravenous line is placed, and the pa ent begins to receive a bolus of 1000 cc of normal saline under pressure. A decision to perform an emergent procedure is made. Immediately after the procedure is performed, the patient is noted to have a dramatic clinical improvement. Subsequent to the procedure, the pa ent has a pulse of 105 bpm, a blood pressure of 95/60 mm Hg, a respiratory rate of 22 breaths/min, and an oxygen satura on of 98% on the nonrebreather mask. The secondary survey is completed, revealing no major injuries. Addi onally, the chest radiograph (see Figure 1) conrms the suspected clinical diagnosis that prompted the emergent procedure.
What is the underlying pathophysiology, and what procedure was performed? Hint: The cause of this patient's hypotension and hypoxia is a clinical diagnosis, and although a portable chest radiograph was performed in this case, this condition should not typically require imaging. o o o o Upper airway obstruction; cricothyrotomy Tension pneumothorax; needle thoracostomy Hypovolumic shock; central line placement Pericardial tamponade; pericardiocentesis
Diagnosis: Tension pneumothorax; needle thoracostomy Discussion: Pneumothorax occurs when air enters the potential space between the visceral and parietal pleura, leading to lung collapse on the affected side. Pneumothoraces may occur spontaneously, especially in the setting of lung disease, or they may result from accidental or iatrogenic trauma. A tension pneumothorax is a life life-threatening condition that occurs when the air in the pleural space is under pressure, displacing mediastina structures and mediastinal compromising cardiopulmonary function. Tension pneumothoraces result from injuries to the lung parenchyma or bronchial tree that can act as one way valves so that air enters the pleural space but cannot escape. The one-way trapped air in a tension pneumothorax causes increased intrathoracic pressure, pushing mediastinal structures contralaterally and reducing venous return and cardiac output. These patients are hypoxic and become difficult to ventilate, with potentially rapid progress to cardiorespiratory collapse and death. Hemothorax is defined by cardiorespiratory blood in the pleural space, and it occurs when the lung parenchyma and the intercostal or mammary vessels are injured. Massive hemothoraces arise with hilar injuries, aortic ruptures, or myocardial ruptu ruptures. A tension hemopneumothorax develops when there is both blood and air under tension in the pleural space space. A pneumothorax in any patient who has sustained thoracic trauma should arouse suspicion. The patient may complain of an acute onset of sharp pleuritic chest pain, with radiation to the ipsilateral shoulder and pleuritic associated dyspnea and anxiety. Typical physical findings in pneumothorax include unilaterally decreased breath sounds, hyperresonance to percussion over the affected lung, and asymmetric ches rise. In tension chest pneumothorax, the patient displays respiratory distress, tachypnea, and tachycardia, and the patient may also experience cyanosis, jugular venous distention, tracheal deviation away from the affected lung, and a pulsus paradoxus. The epidemiology of traumatic pneumothoraces has not been well characterized. In the United States, trauma is demiology the leading cause of death in persons younger than 45 years, and it accounts for approximately 150,000 deaths annually. The overall mortality for thoracic trauma is 10%, and chest injuries cause approximately 1 in 4 trauma thoracic deaths in North America. Pneumothorax is a serious complication of thoracic trauma, and it has been described in 1 in 5 pa ents that survive major trauma. Interes ngly, in one study,2% of pa ents with asymptoma c 1 chest stab wounds had a delayed pneumothorax or hemothorax. While pneumothoraces in stable patients can be confirmed radiographically, a tension pneumothorax causing hemodynamic compromise should be diagnosed clinically, and treatment should never be delayed in favor of diagnostic imaging. A chest x-ray may show a linear shadow of visceral pleura, without lateral lung markings. An ray upright chest x-ray is more sensitive than a supine radiograph, as air tends to accumulate at the lung apex. In ray recumbent patients, air often accumulates in the anterior portion of the inf inferior chest and manifests radiographically as a "deep sulcus." If a pneumothorax without tension physiology is suspected but not seen on the initial upright chest x-ray, a repeat film during exhalation may reveal it. Increasingly, ultrasound is being ray, used as a rapid bedside modality for diagnosing pneumothoraces; some studies have shown that it is more sensitive than radiography for detecting traumatic pneumothoraces. Computed tomography (CT) is more sensitive and specific than chest x x-rays or ultrasonography for the evaluation of small pneumothoraces and hy hemothoraces. Occult pneumothoraces may be present in 2 55% of trauma pa ents, although the clinical 2-55%
Figure 1
What is the diagnosis? Hint The medical history of this patient is significant.
Figure 1
Hint What is that straight line in the right lower lung field?
Figure 1
Two hours later, the nurse pages you because the pa ent's blood pressure had decreased to 75 mm Hg systolic, 50 mm Hg diastolic. Physical examina on reveals diuse and bilateral wheezing with dis nc ve heart sounds. A frontal chest radiograph (A) is obtained.
What should be performed immediately to reverse the hypotension? A. B. C. D. Hint Chest radiograph A reveals hyperinflated lung fields with the endotracheal (ET) tube properly positioned. Starting a dopamine infusion Placing a chest tube Decreasing the ventilator rate Increasing the tidal volume
Figure 1
Hint Signicant features of the history of this pa coronary artery bypass surgery. ent include an appendectomy 12 years ago, hypertension, and
Figure 1
The patient has a normal birth history, no medical problems, and no prior surgeries. Her immunizations are current.On physical examina on, the girl's vital signs are as follows: rectal temperature, 100.2F; pulse, 134 beats per minute; respira ons, 32 breaths per minute; and oxygen satura on with pulse oximetry, 98% on room air. The patient is alert and sitting comfortably with her parents. Her skin and mucous membranes are moist. The remaining findings are normal and reveal a soft, nontender, nondistended abdomen without rebound or guarding. Rectal examination is not performed. While you speak to the parents, the patient clutches her abdomen and cries, doubling over in pain. The episode spontaneously resolves after several minutes. What is the diagnosis? Hint Note the episodic abdominal pain and positive radiographic findings.
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Hint Note the S wave in lead I and the Q wave in lead III.
Figure 1
What is the diagnosis? Hint Children with this idiopathic syndrome often complain of abdominal pain. In some, intussusception or renal dysfunction may even develop. When pressure is placed on the skin lesions, they are palpable but do not blanch.
Figure 1
Which of the following tests would be most helpful in the diagnosis of this case? A. B. C. D. E. Hint The diagnosis is not idiopathic depression. Liver function tests Complete blood count analysis Thyroid-stimulating hormone (TSH) test Urine toxicology screening Rapid plasma reagin (RPR) test
Background A 20-year-old active-duty male soldier presents to the emergency department (ED) of a military hospital complaining of a 3-day history of a dark-red "burning rash." The rash started at his sock line and, over the course of the past 2 days, has spread proximally up his thighs. It is not present on his abdomen or back, but it has spread to his hands over the past day. The patient also developed a sore throat and a scratchy voice the day before presentation, without odynophagia. He was in the North Carolina woods as part of his infantry training, which is supplemental training after boot camp. He reports having spent 20+ hours per day for the past several days in a foxhole (a hole in the ground that soldiers use for protection). The patient reports fatigue only related to his level of activity and lack of sleep during training. He is not taking any medications, he has no allergies, and he has smoked 5-10 cigare es daily for the past year. He also reports drinking approximately 510 beers with his comrades 1-2 mes per month before star ng his training. The pa ent notes some right ankle swelling and pain that started a er a 12.43 mi (20 km) eld hike with a 60 lb (27.22 kg) rucksack on his back. The pain and swelling began 1 month before admission and has worsened in the past few days. He has had no pruritus, fevers, chills, abdominal pain, diarrhea, changes in urine color, or dysuria, as well as no new sexual contacts and no recent animal or insect bites. No one else in his military unit has reported similar skin findings. The patient had a minor motorcycle accident 18 months ago, with a right leg lacera on that required suture repair. He has no significant family history.
Figure 1
On physical examina on, his vital signs demonstrate a strong pulse, with a regular rhythm and a rate of 58 bpm, blood pressure of 123/60 mm Hg, weight of 165.3 lb (75 kg), and oral temperature of 98.1F (36.7C). He is a very fit, well-developed white male in no apparent distress. The pharynx shows no erythema or exudate, and the neck examination demonstrates no tenderness to palpation or lymphadenopathy. The cardiac examination is notable for a point of maximum intensity at the 5th le interspace, but nomurmurs, gallops, or rubs are appreciated. The patient's pulses are strong bilaterally. The respiratory examination reveals lungs clear to auscultation bilaterally. The abdominal examination is unremarkable, and the stool test is negative for occult blood. The skin examina on show lesions ranging in diameter from 2 mm to 10 cm (see Figures 13). The macules and plaques are nonblanchable, and most of them are concentrated in the posterior calves, the palms,
Figure 2
A urinalysis shows 2+ protein and 2+ blood, with 25-50 red blood cells (RBCs) per high-power field on microscopy. His coagulation studies at admission include a prothrombin me (PT) of 12.3 s, an interna onal normalized ra on (INR) of 1.08, and a par al thromboplas n me (PTT) of 25.5 s. The pa ent's blood urea mol/L). The complete nitrogen (BUN) is 24 mg/dL (8.59 mmol/L) and his crea nine value is 1.1 mg/dL (97.2 blood count (CBC) shows a white blood cell (WBC) count of 7.4 103/L (7.4 109/L), a hemoglobin (HGB) of 12.4 g/dL (124 g/L), a hematocrit (HCT) of 37.1% (0.371), and a platelet count of 195 103/L (195 109/L), with a normal smear. Skin punch biopsies of 2 of the lesions are obtained that demonstrate small-vessel leukocytoclastic vasculitis. Immunofluorescence of the skin biopsies demonstrates a weak linear pattern at the dermal-epidermal junction for immunoglobulin G (IgG), immunoglobulin A (IgA), and complement 3 (C3).
Figure 3
Diagnosis: Henoch-Schnlein purpura (HSP) Schnlein Discussion: There exist several guidelines for the diagnosis of Henoch Schnlein purpura. The American College of Henoch-Schnlein Rheumatology (ACR) requires 4 criteria (published in 1990) for diagnosing Henoch-Schnlein purpura: palpable es Henochpurpura, pa ent age of 20 years or less at onset, bowel angina, and the presence of granulocytes in the vessel walls. More recently, in 2006, the European League Against Rheumatism (EULAR) and the Pediatric Rheumatism Rheumatology Society published their own Henoch Schnlein purpura criteria. These include palpable purpura Henoch-Schnlein as a mandatory criterion, with at least one of the following conditions: diffuse abdominal pain, predominant IgA deposition (confirmed on biopsy), acute arthritis in any joint, and renal involvement (as evidenced by hematuria and/or proteinuria). According to the older ACR criteria, the diagnosis of Henoch Henoch-Schnlein purpura for our patient could be called into question, as he exhibited no bowel angina; however, according to the more recent on, EULAR criteria, our patient fits the diagnosis of Henoch Schnlein purpura quite well, as he has palpable Henoch-Schnlein purpura, predominant IgA deposition confirmed on biopsy, a monoarticular arthralgia in his right ankle, and arthralgia renal involvement. The sine qua non for the diagnosis of Henoch Schnlein purpura is a skin biopsy finding of IgA deposition at the Henoch-Schnlein dermal-epidermal junction. A skin biopsy with immunofluorescence studies is recommended if clinical suspicion epidermal of Henoch-Schnlein purpura exists. The etiology of the disease remains unknown, but it is understood to be an Schnlein autoimmune response (usually to an upper respiratory infection). Other items in the differential diagnosis include many of the etiologies of palpable purpura. An algorithmic a empt has been made (see Table 1) to delineate these e ologies, but classica on remains dicult.Palpable purpura is a classic skin manifestation of cutaneous vasculitis, but there are many other entit that can cause entities it. Additional information can be gleaned from the pathologic diagnosis of small vessel vasculitis, which also carries its own dieren al (see Table 2). The intersec on of these 2 dieren als consists of the following set of diagnoses: mixed cryoglobulinemia, vasculitis associated with collagen vascular disease (ie, systemic lupus es: erythematosus, rheumatoid arthritis), and Henoch Henoch-Schnlein purpura. Mixed cryoglobulinemia was easily ruled out, as the patient's serum cryoglobulin test a complement levels and were a C3 of 118 mg/dL (1.18 g/L; normal range, 79 152 mg/dL), a C4 of 26 mg/dL (0.26 g/L; normal range, 16 79-152 1638 mg/dL), complement CH50 of 53.0 U/mL (53 kU/L; normal range 22 60 U/mL), and a nega ve serum 22-60 cryoglobulin examination. Another diagnosis that was readily excluded was systemic lupus erythematosus. Our her pa ent had only 1 arthralgia, but no fevers, myalgia, or malaise were noted; only 1/11 American Rheumatologic Association criteria for the diagnosis of lupus were met. To satisfy the clinical diagnosis of systemic lupus satisfy erythematosus, 4/11 American Rheumatologic Associa on criteria are required. Although the pa ent meets the histopathologic criteria for solitary IgA nephropathy, as the renal biopsy showed diffuse proliferative endocapillary glomerulonephritis with increased mesangial matrix and cellularity, capillary wall thickening, and lobular accentua on on light and electron microscopy with strong (3+) mesangial staining for IgA and fibrinogen, as well as lappa and lambda l light chains (2-3+) present on immunouorescence microscopy, he also 3+) exhibited some of the cardinal clinical features of Henoch Schnlein purpura at presentation. He denied having Henoch-Schnlein
Table 1: E
ology of Purpura
Alterations in platelet formation, destruction, or function Drugs (aspirin, methyldopa) Idiopathic thrombocytopenic purpura Thrombotic thrombocytopenic purpura Disseminated intravascular coagulation Infection (especially Neisseria, Rickettsia, Staphylococcus) Splenic sequestration Radiation therapy Myelofibrosis Myeloproliferative disorders Cutaneous vasculitis Purely cutaneous vasculitis (eg, secondary to medications) Henoch-Schnlein purpura Polyarteritis nodosa Granulomatous vasculitis (Wegener granulomatosis, Churg-Strauss vasculitis) Cutaneous vasculitis associated with a collagen Vascular disease (eg, systemic lupus erythematosus, rheumatoid arthritis) Giant cell arteritis Mixed cryoglobulinemia Hyperglobulinemic purpura Trauma Subacute bacterial endocarditis Other embolic diseases Amyloidosis Corticosteroids Toxins and venoms Senile purpura Scurvy Valsalva maneuver Pseudopurpura (Sweet syndrome, cherry angiomas, angiokeratoma, Kaposi sarcoma)
zing Vasculi
Hypersensitivity vasculitis Henoch-Schnlein purpura Essential Mixed Cryoglobulinemia Vasculitis associated with connective tissue disease Vasculitis associated with malignancy Serum sickness and serum sickness-like reactions Chronic urticaria (urticarial vasculitis) Urticarial prodrome of acute hepatitis type B infection
Nodules, bullae, or ulcers Large Vessels Signs Subcutaneous ecchymoses nodules, ulceration, and,
Diseases
Polyarteritis nodosa Churg-Strauss syndrome Wegener granulomatosis Giant cell (temporal) arteritis
Figure 1
Today, while preparing to board a plane, he developed a worsening headache, bilious emesis, palpitations, and sweats. He decided to delay his trip and is now presenting to the local ED for further evaluation. The patient denies having any trauma, seizures, abdominal pain, stiff neck, or photophobia. He has no significant past medical history, and his only medica on use is the ibuprofen that he has taken over the past 2 days. On physical examina on, his temperature is 103.0 F (39.4 C), his pulse is 83 bpm, his blood pressure is 120/70 mm Hg, his respiratory rate is 16 breaths/min, and his oxygen satura on is 96% while breathing room air. The patient is generally well-appearing, alert, and oriented. The examination of the head, eyes, and pupils is unremarkable. The neck is supple, without any lymphadenopathy. On auscultation, the lungs are clear; additionally, the patient's heart has a regular rate and rhythm, without any murmurs. The examination of the abdomen reveals normal bowel sounds, with mild tenderness to palpation in the right and left upper quadrants. The spleen is noted to be 3 cm below the costal margin. The neurologic examina on is unremarkable.
Diagnosis: Malaria Discussion: This case is an example of malaria caused by Plasmodium falciparum. In the context of the patient's recent . travel to Nigeria and presentation with fever, malaria was strongly suspected. The patient's blood smear was notable for 15% parasitemia, most likely P falciparum (as evidenced by the circles within some of the red blood cells [RBCs] in the smear seen in Figure 2). The other laboratory ndings, such as the thrombocytopenia and elevated bilirubin, correlated with the disease burden. The elevated creatinine value was also noted, as this creatinine finding is sometimes seen in more aggressive cases of the disease; however, this usually resolves with time. Worldwide, there are about 300-500 million new cases of malaria annually. Malaria is the most deadly vector 500 vectorborne illness in the world, causing 3.5 5 million deaths annually. On average, 40% of the 50 million people who 3.5-5 travel from industrialized to developing countries each year report some illness associated with their travel. developing Approximately 1,200 cases of malaria are reported each year in the United States among travelers; therefore, it is important to consider malaria as a possible cause of fever in the returning traveler. Malaria results from an infec on caused by any of the following 4 protozoa of the genusPlasmodium: falciparum, vivax, ovale and malariae. Transmission of the parasite occurs via the bite of the Anopheles malariae. mosquito. Once the protozoa are injected into the bloodstream, they enter the hepatic cells and reproduce; re eventually, the hepatic cells erupt and release more protozoa into the host's circulation. These parasites then remain in the bloodstream, periodically invading erythrocytes, causing hemolysis, and infecting new RBCs. causing The incuba on period tends to be 918 days for P falciparum, P vivax and P ovale but P malariae has an ovale, incuba on period of 1840 days. The most common parasites seen in the US are P falciparum, which is often found in travelers returning from Sub d Sub-Saharan Africa, and P vivax, which is found in those returning from Asia, , Eastern Europe, and La n America. The clinical presenta on also varies between these 2 parasites:falciparum P often causes symptoms within the first month following the travel period, and it can be fatal; of patients first infected with P vivax, 50% have symptoms within 1 month a er travel, and approximately 2% of pa ents may , have symptoms 1 year a er exposure. The majority of pa ents infected with ither parasite are usually e symptoma c within the rst 3 months a er they return to the US. The clinical presentation of malaria can vary widely and depends on the species of Plasmodium involved. Common symptoms include fever, malaise, myalgias, and headache, which may be accompanied by cough, headache, abdominal pain, or diarrhea. Since these symptoms are non specific, malaria should be considered in all febrile non-specific, travelers, regardless of their clinical presenta on. In fact, approximately 78100% of pa ents presening with t malaria are febrile when they are first examined. The classically described fever patterns are rarely observed; however, when these fevers do occur at 48 to 72-hour intervals, this finding is virtually pathognomonic for P 48hour vivax, P ovale, and P malariae infections. This cyclical pattern of symptoms coincides with the regular interval of erythrocyte hemolysis. On examina on, splenomegaly is found in 2448% of pa ents, and pa ents may complain of abdominal pain. Severe malaria, usually caused by P falciparum, causes several manifestations, , including prostration, impaired consciousness or coma, respiratory distress caused by pulmonary edema and acute respiratory distress syndrome (ARDS), seizures, circulatory collapse, abnormal bleeding (including
Figure 1
The pain started about 4 hours before presenta on to the ED and has been persistent; it is present in the upper abdomen and is centered in the epigastrium. He describes the pain as deep and burning. There is no associated nausea or vomiting. He does not report any changes in his bowel habits and has not experienced any recent fevers. The review of systems is also negative for any recent unintended weight loss or trauma. The patient also reports having had "indigestion" in the past that caused pain similar to what he is currently experiencing, though much less in intensity. His past medical history is significant for coronary artery disease and hypertension. He takes two medications, both for his high blood pressure, but does not drink excessively and does not smoke. On physical examination, the patient is pale and in obvious severe discomfort. His heart rate is 122 bpm, and his blood pressure is 110/65 mm Hg. He is breathing with rapid shallow breaths at a rate greater than 30 breaths/min. His temperature is normal at 99.2F (37.3C), and a pulse oximetry reading while the patient is breathing room air shows a satura on rate of 100%. The cardiovascular and respiratory ndings are unremarkable. The patient has significant tenderness in the epigastric region, with a rigid abdomen. There is little to no tenderness to palpation in the lower quadrants; a reliable assessment of the upper quadrants is not possible because of the tenderness in the epigastric region. Hyperactive bowel sounds are heard on auscultation. The patient's stool is brown and guaiac positive. An electrocardiogram is performed and is noted to be unremarkable except for sinus tachycardia. A complete blood count (CBC) and a chemistry panel are sent. The CBC reveals a mild anemia, with a hemoglobin concentra on of 127 g/L (12.7 g/dL). On the chemistry pane there is evidence of a slight azotemia, with a l, blood urea nitrogen level (BUN) of 17.1 mmol/L (48 mg/dL) and a crea nine value of 106 mol/L (1.2 mg/dL). The remainder of the laboratory investigations are unremarkable. Plain radiographs of the abdomen are performed (see Figures 1A and 1B).
Diagnosis: Pneumoperitoneum from duodenal ulcer perforation Discussion: Clear deni on of both the inner wall and outer wall of the bowel on Figure 2A (the Rigler sign; see below for explanation) and the presence of free air under the right hemidiaphragm on Figure 2B demonstrate n) pneumoperitoneum. The term "pneumoperitoneum" refers to air in the peritoneal cavity. The differential diagnosis of pneumoperitoneum includes iatrogenic causes (eg, peritoneal dialysis; abdominal surgery, peritoneal including laparoscopy and laparotomy, a er which pneumoperitoneum can persist for up to 28 days), blunt or penetrating trauma, perforation of the hollow viscera (eg, gastric ulcer, duodenal ulcer), pneumatosis intestinalis or pneumatosis coli, vaginal insufflation, and gas from the mediastinum (eg, from barotrauma). lis Although many patients with a perforated peptic ulcer initially present with severe abdominal pain as well as epigastric tenderness and classic signs of peritonitis, patients who are elderly, are immunocompromised, or peritonitis, have an altered mental status may have only minimal signs and symptoms. In one study of pa ents >60 years with perforated ulcers, only 70% had abdominal pain. Other pa ents reported symptoms tht included a dyspepsia, anorexia, nausea, and vomi ng. Severe abdominal pain was present in only 16% of pa ents. About 6% of pa ents with perforated ulcers have no abdominal ndings. In most cases of perfora on from ulcer disease, gastric and duodenal content (ie, bile, ingested food, swallowed bacteria) leaks into the peritoneum, resulting in peritonitis and an increased risk of infection and abscess formation. In addition to sepsis, subsequent third-spacing of fluid into the peritoneal cavity caused by the peritonitis can lead to hypotension spacing by and shock. The underlying pathophysiology of a duodenal ulcer is a common condition that is characterized by the presence of a well-demarcated mucosal defect in the duodenum. Approximately 95% of duodenal ulcers ar demarcated are found in the rst part of the duodenum; most are less than 1 cm in diameter. A prompt and accurate diagnosis combined with treatment can effectively prevent potentially serious complications, such as perforation (which occurred in this case). The duodenal mucosa resists damage from the effects of gastric acid and the proteolytic al enzyme pepsin as a result of the protective qualities of the mucous/gel layer produced by the mucus mucus-secreting epithelial cells, bicarbonate secretions from other gastric and duodenal cellular components, and protective duodenal prostaglandins. If gastric acid and pepsin penetrate the mucous layer and reach the epithelial cells, ion pumps in the basolateral cell membrane regulate intracellular pH by removing excess hydrogen ions; healthy ep epithelial cells migrate to the site of the injury; and mucosal blood flow serves to remove any excess acid diffused through the injured mucosa. Despite these barriers and mechanisms to prevent permanent injury, ulcerations can occur. Any pathophysiologic or iatrogenic process that increases gastric acidity (eg, disease states with increased maximal and basal acid output), decreases prostaglandin production (eg, nonsteroidal anti anti-inflammatory drug [NSAID] use, which leads to inhibition of the cyclooxygenase [COX-1] pathway), or interferes with the mucous cyclooxygenase-1 1] layer (eg, Helicobacter pylori infection leading to stimulation of gastric acid production) can result in the formation of peptic ulcer disease. In the US, the prevalence of duodenal ulcer is es mated to be 615% in the general popula on. The majority of individuals with duodenal ulcers do not have clinically significant disease. The prevalence is closely linked to the presence of H pylori infection. Of those individuals infected with H pylori, the lifetime prevalence is ion. ,
Figure 1
On physical examination, his vital signs are signicant for a respiratory rate of 70 breaths/min and a heart rate of 296 bpm. He is afebrile, with a rectal temperature of 98.2F (36.8C). His blood pressure is 72/40 mm Hg. His a oxygen satura on, measured by pulse oximetry, is 98% while brething room air. Despite the abnormal vital signs, the baby does not appear distressed or even uncomfortable. He is moving all extremities, and he opens his eyes and looks around. His oropharynx is clear, with no visible foreign bodies. There is no rhinorrhea or nasal congestion. His lung sounds are clear, and despite the significant tachypnea, no retractions, grunting, or nasal flaring are present. On auscultation of the heart, rapid heart sounds are noted, and as a result of the tachycardia, an assessment for murmurs is not possible. His distal extremities are pink and have a normal capillary refill.While placing an intravenous line and connecting the child to a monitor, an electrocardiogram (EKG) is obtained.
What type of arrhythmia is shown on the EKG? Hint: Consider the morphology of the QRS complexes (narrow vs wide) and the timing of the complexes (regular vs irregular). o o o o Torsade de pointes Atrial fibrillation Supraventricular tachycardia Ventricular tachycardia
Diagnosis:Supraventricular tachycardia Supraventricular Discussion: This patient was diagnosed with supraventricular tachycardia (SVT), which is defined as a regular, rapid rhythm that requires only atrial or atrioventricular tissue for its initiation and maintenance. Paroxysmal SVT (PSVT) is the most common dysrhythmia in children. It has an interna onal prevalence of about 2 cases per 1,000 people. PSVT tends to manifest in infancy and early childhood. The presentation of PSVT is quite variable in children, ranging from an incidental finding in an asymptomatic resentation patient to fulminant cardiogenic shock. Infants present with caretakers complaining of rapid breathing, poor feeding, sweating with feeding, pallor, lethargy, and excessive crying. Older children may complain of chest lethargy, pain, shortness of breath, and palpitations. The physical examination is likewise variable, depending upon the child's age and heart rate and on the duration of the episode (which can last from seconds to days). For infants, the examination is remarkable for a regular tachycardia. Normal resting heart rates for neonates can be up to 160 beats per minute. The upper limit of the normal heart rate decreases with age un l late adolescence, when children's heart rates are similar to those of adults. Heart rates ranging beyond the normal upper limits, par cularly in excess of 240, should be highly suspicious for SVT. In addi on to tachycardia, infants may have physical findings of pallor, irritability, lethargy, tachypnea, weight loss (or failure to gain), poor perfusion, weak bility, pulses/hypotension, hepatomegaly, and, sometimes, cardiogenic shock. A pounding sensation in the neck may be caused by cannon A waves, which occur when the atrium contracts at the same time as the ventricle. Older children typically have benign examinations (except for the findings of tachycardia and tachypnea). There are 3 types of SVT: (1) atrial tachycardia (ectopic, or nonreciproca ng, atrial tachycardia), (2) atrioventricular nodal reentrant tachycardia (AVNRT), and (3) atrioventricular reentrant (or reciproca ng) ricular tachycardia (AVRT). In the United States, reentrant tachycardias are the most common cause of PSVT in the pediatric population, with AVRT being more common than AVNRT. AVRT consists of 2 or more func onally (and, than usually, anatomically) distinct pathways between the atria and ventricles. The first pathway is usually the atrioventricular (AV) node. The second is an accessory pathway that may be an anatomically separate bypass tract between the atrium and ventricle (such as the bundle of Kent). Wolff Parkinson-White (WPW) syndrome Wolff-Parkinson preexcitation is a good example of SVT caused by an anatomically separate bypass tract. Each pathway has different electrophysiologic characteristics; one pathway is fast (a short conduction time and a long refractory period), while the other is slow (a longer conduction time and a shorter refractory period). In AVNRT, both pathways exist in the AV node itself. In AVNRT, for example, while the child is in regular sinus, a premature while atrial beat may block in the fast pathway (because of its longer refractory period). Since the fast pathway is blocked, the signal conducts down the slow pathway. Then, when the impulse reaches the insertion of the fast pathway, which has now recovered after its refractory period, the impulse conducts in a retrograde fashion through the fast pathway. This results in a circuit loop tachycardia, with an impulse moving in a loop down the slow pathway and up the fast one. Other causes of PSVT include sympathomimetic stimulation (such as medications for upper respiratory infection), structural defects, and atrial ectopy. About half of all SVT cases occur without underlying heart disease; these cases are termed idiopathic. Idiopathic SVT is more common in younger patients than in older idiopathic.
Figure 1
On physical examina on, the pa ent is afebrile and has a pulse of 72 bpm, a blood pressure of 130/82 mm Hg, a respiratory rate of 12 breaths/min, and a normal oxygen satura on while breathing room air.He is welldeveloped and well-appearing. Examination of the anterior neck reveals a nontender, nonerythematous, uctuant mass measuring approximately 10 8 cm in the midline of the lower neck, with slight extension to the right side of the midline. The mass moves up and down when the patient swallows, and it slightly displaces anteriorly with protrusion of the tongue. No cervical lymphadenopathy is appreciated. The lung fields are clear bilaterally, without any evidence of stridor or wheeze. The heart has a regular rate and rhythm, without murmurs, and the abdomen is soft and nontender, without evidence of masses. The cranial nerves are intact, and the remainder of the neurologic exam is unrevealing as well.
Figure 2
What is the diagnosis? Hint: This is the most common congenital anomaly resulting in a midline neck mass. o o o o Cystic vascular abnormality Cervical teratoma Ectopic thyroid Thyroglossal duct cyst
Diagnosis: Thyroglossal duct cyst Discussion: The ultrasound image in Figure 1 shows a large cys c mass anterior to the thyroid gland (arrowheads). The contrast-enhanced CT scan (Figure 2) demonstrates that same predominantly midline cystic mass extending enhanced anteriorly to the thyroid gland and under the strap muscles, without any evidence of ectopic thyroid tissue. The findings are consistent with the diagnosis of a thyroglossal duct cyst. This diagnosis is the most common etiology for a midline neck mass. Thyroglossal duct cysts usually occur between the hyoid bone and the thyroid gland, and they represent up to 70% of congenital neck anomalies. Thyroglossal duct cysts are second only to lymphadenopathy as the most common cause of a neck mass. ost The cysts usually appear in the midline and can be present anywhere along the line of fetal descent from the foramen cecum to the level of the thyroid gland. From an embryologic perspective, the thyroid gland develops during the third week of life as an outgrowth of the floor of the primitive pharynx. The primitive thyroid then g descends from the foramen cecum to its mature position in the anterior neck through the thyroglossal duct. The thyroglossal duct is normally resorbed by 7 to 10 weeks of fetal life. Abnormal persistence of the thyroglossal tract accompanied by mucus production from the endothelial lining of the tract leads to the development of a thyroglossal duct cyst. Approximately 7% of the popula on has thyrogloss duct remnants, and the distribution al is equal among males and females. The cysts are usually found in children or adults younger than age 30 years, but they can develop in adults of any age. In recent years, a number of older patients, including patients in their 80s and 90s, have presented with thyroglossal duct cysts. There are 4 general types of thyroglossal duct cysts: thyrohyoid (61% of cases), suprahyoid (24%), suprasternal (13%), and intralingual (2%). The differential diagnosis for neck masses can be categorized by the location of the mass itself; the usual categorization is between lateral and midline masses. The most frequent causes of lateral masses are lymphadenopathy, branchial cleft cyst malignancy, cystic lymphangioma, and dermoid and terato cysts. teratoid Although thyroglossal duct cysts are the most common etiology for midline masses, the differential diagnosis also includes dermoid and teratoid cysts, ectopic thyroid tissue, malignancy, and cystic lymphangiomas. On radiologic images, thyroglossal duct cysts appear as a cystlike mass along the course of the thyroglossal duct. l They must be differentiated from dermoid cysts and lymphangiomas. A dermoid cyst usually contains fat; lymphangioma is most common in infancy or early childhood, and it usually occurs in the posterior triangle of usually the neck, behind the sternocleidomastoid muscle. A thyroglossal duct cyst must also be differentiated from an ectopic thyroid gland. If an ectopic thyroid gland is mistakenly removed, the patient may require long long-term thyroid treatment for hypothyroidism. Often, patients with an ectopic thyroid also have hypothyroidism, and they will have an elevated thyroid-stimulating hormone (TSH) level. stimulating The diagnosis of thyroglossal duct cyst is made on the basis of the clinical history and confirmed with diagnostic imaging. Most patients with thyroglossal duct cysts present with either a history of a slowly growing, asymptomatic mass or of a relatively r rapid-growing mass (if the cyst is infected) in the anterior midline of the growing neck. Frequently, the swelling is exacerbated during an upper respiratory infection. The pathognomonic sign of
Figure 1
On physical examina on, the pa ent is afebrile, with a pulse of 65 bpm, a blood pressure of 120/84 mm Hg, and a respiratory rate of 15 breaths/min. His room air satura on reading is 100%. In general, he is well -appearing and in no acute distress. The patient's neck examination shows no jugular venous distention. The heart sounds, including S1and S2, reveal no audible murmurs, rubs, or gallops. The apical impulse is nondisplaced and of normal impact. The lung sounds are diminished throughout, but there are no wheezes, rales, or rhonchi. He has no edema of the lower extremities, and the distal pulses are easily palpable. All other exam findings, including a neurologic examination, are unremarkable. The pa ent is placed on a cardiac monitor, and an 18gauge intravenous (IV) catheter is inserted into the antecubital fossa. Laboratory tests consisting of a complete blood count (CBC) and serum electrolytes are ordered. A portable chest radiograph reveals slight hyperinflation and hyperlucency of the lung fields, with a flattened diaphragm and central pulmonary artery enlargement. An electrocardiogram (ECG) is obtained (see Figure 1).
Diagnosis: Wolff-Parkinson-White syndrome White Discussion: Preexcitation is characterized by an accessory pathway within the heart that conducts action potentials between the atria and ventricles outside of the normal conduction system (which conducts through the atrioventricular [AV] node-His-Purkinje system). The phenomenon was dened by Durrer et al in 1970, who Purkinje stated that "preexcitation exists, if in relation to atrial events, the whole or some part of the ventricular muscle is activated earlier by the impulse originating from the atrium than would be expected if the impulse reached pulse the ventricles by way of the normal specific conduction system only. Of the various types of preexcitation syndromes, the most common is Wolff Wolff-Parkinson-White (WPW) syndrome.
Figure 1
WPW syndrome can be identified by a classic fusion QRS complex ECG pattern that is a combination of simultaneous normal conduction through the AV node and aberrant conduction through the accessory tract. This fusion QRS complex leads to par cular ECG features that include a shortened PR interval (<120 msec) and a widened QRS complex with a delta wave representing preexcitation of the ventricle through the accessory pathway. The distinctive ECG pattern of the accessory pathway was initially described by Wolff, Parkinson, and initially White in 1930 as a bundle branch block with a short PR interval. Addi onally, as men oned, WPW syndrome is recognized as the most common form of ventricular preexcitation, although it likely represents a collecti of collection pathologic conditions rather than a single structural abnormality.
Figure 2
On evaluation in the emergency department, the patient was asymptomatic except for a persistent cough with clear sputum. She was a nonsmoker and had no previous pulmonary disease. She did not have a history of tuberculosis or known exposure to risk factors. A purified protein derivative of tuberculin (PPD) test performed 3 months ago yielded nega ve resul She has not been taking any drugs and has no known allergies. Physical ts. examination revealed a well-appearing woman in no distress with a respiratory rate of 16 breaths per minute, a temperature of 35.9C, a blood pressure of 110/60 mm Hg, and a heart rate of 95 beats per minute. Her lungs were clear, with no wheezing, rhonchi, or rales. Her heart sounds were normal, with no murmurs. The remainder of her examination yielded unremarkable findings.
Figure 3
Chest CT was performed (see Image). Positron emission tomography (PET) showed increased uptake in the left posterior por on of the lower lung with a standard uptake value (SUV) of 6.5 and no uptake in the nodules or hilar or mediastinal nodes.
What is the diagnosis? Hint The patient's indolent presentation is typical of this condition.
Figure 4