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A 56-year-old man comes to the office for follow up of hypertension. The patient had undergone kidney transplantation one year ago for focal segmental glomerulosclerosis. He was originally seen in the office 8 weeks ago for hypertension and had a blood pressure of 210/110 mm Hg, initially he was given amlodipine, but the patient continued have hypertension. Two weeks ago, he was also started on lisinopril. In addition, he takes tacrolimus and low-dose prednisone. The patient currently feels well. Today, blood pressure is 160/90 mm Hg, pulse is 78/min, and respirations are 16/min. Examination shows normal jugular venous pressure, vesicular breath sounds, and normal heart sounds. The transplant site is nontender Laboratory studies reveal a serum creatinine level of 2.4 mg/dL (2 weeks ago: 1.5 mg/dL) Serum tacrolimus level is within the normal therapeutic range.

Explanation

This patient with a history of renal transplant has severe, persistent hypertension. In association with the acute kidney injury (AKI) that developed after initiation of lisinopril, this presentation suggests renovascular hypertension due to transplant renal artery stenosis (RAS). Although most cases of RAS occur in elderly men with diffuse atherosclerotic disease, it can also occur in patients with a transplanted kidney and is commonly associated with operative abnormalities (eg, trauma during organ procurement, abnormal suture placement), viral infection (cytomegalovirus, BK virus), and atherosclerosis of the donor artery. Transplant RAS typically occurs in the first 2 years after transplantation.

Similar to RAS due to other causes, transplant RAS typically manifests with resistant hypertension. A decline in renal function after the addition of ACE inhibitors or angiotensin II receptor blockers is highly suggestive of the diagnosis. Other findings that suggest RAS include a lateralizing abdominal bruit and recurrent flash pulmonary edema. The diagnosis is made with renal vascular imaging (eg, renal Doppler ultrasonography). Management of transplant RAS usually includes angioplasty, possibly with stent placement.

(Choice A) Kidney biopsy is indicated to evaluate for AKI due to acute allograft rejection, which is somewhat less likely in the absence of graft tenderness or fever. In addition, biopsy is invasive, and noninvasive methods of assessment (eg, imaging) should be performed prior to biopsy.

(Choice B) Because transplant RAS is the equivalent of bilateral RAS in a non-transplant patient, the initiation of an ACE inhibitor is likely to trigger AKI. Increased lisinopril dosing would likely further worsen this patient's renal function.

(Choices C and E) High-dose prednisone is a common cause of hypertension, however, low doses are not typically associated with marked hypertension. Toxicity to calcineurin inhibitors (eg, tacrolimus) can cause hypertension and AKI; however, such adverse effects are more common with elevated plasma drug levels. In addition, the timing of this patient's AKI following initiation of lisinopril makes RAS more likely than an adverse effect of immunosuppression.


Points To remember On Finger Tips

Renal artery stenosis (RAS) can occur in the renal allograft, typically within 2 years of transplant. Like other forms of RAS, suggestive findings include persistently elevated blood pressure, decline in renal function with the addition of ACE inhibitors, a lateralizing abdominal bruit, and recurrent flash pulmonary edema. The diagnosis is made with renal vascular imaging (eg, renal Doppler

A 22-year-old woman comes to the emergency department due to abdominal pain. The patient has had intermittent abdominal pain for the past 2 days, but today the pain has worsened and become constant. She has had no nausea, vomiting, or change in bowel or bladder patterns. The patient's medical history is significant for sickle cell disease, for which she is prescribed hydrocodone as needed; she began taking multiple hydrocodone tablets today when the pain got worse but had only minimal relief. Her last menstrual period was 4 months ago, and she has multiple sexual partners. Temperature is 37.1 C (98.8 F), blood pressure is 132/88 mm Hg, and pulse is 90/min. The abdomen is diffusely tender to deep palpation, there is no rebound or guarding. On pelvic examination, the uterus is enlarged and nontender and the cervix is closed. The remainder of the examination is unremarkable. Pelvic ultrasound reveals an intrauterine pregnancy at 12 weeks gestation with a fetal heart rate of 160/min. Bilateral adnexa have normal Doppler blood flow.
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This patient at 12 weeks gestation with abdominal pain is likely having an acute pain episode (ie, vasoocclusive pain crisis) due to sickle cell disease (SCD) Acute pain episodes are more common in pregnancy, likely because of increased metabolic demands and a hypercoagulable state Although the incidence typically increases with gestational age, acute pain episodes can occur in the first trimester, especially if there are other precipitating factors (eg, stress, nausea/vorniting, dehydration)

Acute pain episodes can last from hours to days and commonly involve the chest, abdomen (as in this case), or long bones. Pain occurs due to

repetitive red blood cell sickling, which causes microvascular occlusion, decreased perfusion, and tissue ischemia (eg, abdominal tenderness)

Management is with fluid resuscitation and opioid pain control

in addition to an increased risk of acute pain episodes patients with SCD are at increased risk of preeclampsia and its sequelae, including placental abruption, fetal growth restriction, and preterm delivery. Therefore, these patients require more frequent prenatal care, a baseline 24 hour urine protein level, and low-dose aspinn for preeclampsia prophylaxis

(Choice A) Opioid use and pregnancy are risk factors for constipation due to decreased gastrointestinal motility, however, this patient's pain

preceded her hydrocodone use, and no changes in bowel pattern are present. (Choice B) Ovarian torsion classically presents with intermittent abdominal pain that suddenly becomes constant and severe due to decreased

ovarian blood flow (evidenced on ultrasound) This patient has normal Doppler blood flow to the adnexa

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(Choice C) Having multiple sexual partners is a risk factor for pelvic inflammatory disease (PID), which can cause diffuse abdominal tenderness However, PID also typically causes fever and uterine tendemess. In addition, PID is uncommon in pregnancy because the cervical mucus plug usually protects the uterus from ascending bacteria

(Choice D) Round ligament pain, caused by the ligament being stretched by the gravid uterus, typically presents as a sharp pain that radiates to

the vagina, not as diffuse abdominal pain

(Choice F) Patients with SCD are at increased risk for spontaneous abortion, however, this patient has a closed cervix, a normal fetal heart rate, and no vaginal bleeding, making this diagnosis less likely

Points To Remember on Finger Tips

During pregnancy, patients with sickle cell disease have an increased incidence of acute vascocclusive pain episodes (eg, abdominal pa increased metabolic demands and a hypercoagulable state
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A 43-year-old woman comes to the emergency department due to nausea, dizziness, and headache for a day. Her menses began 2 days ago. She has occasionally had fatigue and dizziness during her menstrual periods, but today's symptoms feel different. The patient has a history of von Willebrand disease, causing recurrent, heavy menstrual blood loss, and is scheduled for an endometrial ablation procedure. Her only medication is intranasal desmopressin taken on the first 3 days of her menstrual period. Temperature is 36.9 C (98.4 F), blood pressure is 120/80 mm Hg, pulse is 92/min and regular, and respirations are 18/min. The patient appears restless. Mucous membranes are moist. Deep tendon reflexes are 2+ throughout and Babinski sign is absent. Sensory examination shows no focal deficits. The chest is clear to auscultation. The abdomen is soft and nontender. There is no peripheral edema. The remainder of the examination is unremarkable.

This patient's acute nausea is likely due to hyponatremia induced by recent use of intranasal desmopressin Desmopressin is an analogue of antidiuretic hormone (ADH) commonly used to treat central diabetes insipidus, it also promotes the release of von Willebrand factor, and can treat mild to moderately heavy menstrual bleeding associated with von Willebrand disease. However, since desmopressin induces physiologic effects of ADH (eg, renal water reabsorption, concentration of urine), it can cause hyponatremia and excess ADH stimulation, manifesting as syndrome of inappropriate ADH secretion (SIADH). Therefore, serum electrolytes should be obtained first in this patient to check for hyponatremia and rule in the diagnosis of SIADH.

Expected laboratory findings in patients with SIADH include hypotonic hyponatremia (due to ADH-mediated water retention and reabsorption), high urine osmolality (ie, concentrated urine), and high urine sodium (due to increased secretion of natriuretic peptides). seen in this patient, SIADH is also associated with euvolemia (eg, absence of edema or jugular venous distension) on physical examination. At first, ADH mediated water reabsorption slightly increases extracellular volume, however, increased natriuretic peptide secretion leads to sodium and water excretion, ultimately normalizing extracellular volume.

(Choice A) Although hypoxemia (eg, from pulmonary embolism) may manifest with nausea, elevated heart rate, and dizziness, this patient has no risk factors for pulmonary disease or symptoms of respiratory distress (eg, shortness of breath, chest pain). Therefore, serum electrolytes are a better initial test

(Choice B) Although acute liver failure may cause excessive bleeding and present with nausea and dizziness, this patient lacks associated findings of jaundice and abdominal pain and has no risk factors (eg, infection, excess alcohol intake).

(Choice C) MRI of the brain can be used to assess for CNS pathology (eg, bleeding, acute stroke) that could manifest with headache or dizziness. However, this patient lacks focal neurologic signs, therefore, a metabolic workup with serum electrolytes is a more appropriate initial test.

(Choice D) Plasma desmopressin is not routinely measured. It may be high in this patient, given her recent medication use with the onset of menses, but serum electrolytes are a more rapid initial step for confirming hyponatremia and SIADH.

Things to remember👇👇
The administration of desmopressin, an analogue of antidiuretic hormone (ADH), can induce the syndrome of inappropriate ADH secretion. Urinary water excretion is impaired, leading to hypotonic hyponatremia. Laboratory studies, including serum electrolytes, urine osmolality, and urine sodium, are the first step in establishing the diagnosis.

A 4-year-old girl is brought to the ED due to severe oral pain. The patient's pain began 2 weeks ago with discomfort while chewing, and has progressively worsened to refusing any oral intake. She had a similar episode of oral pain last year. Medical history includes 2 sinus infections and numerous episodes of cellulitis. Skin cultures from her previous infections isolated Staphylococcus aureus and Streptococcus pyogenes. Physical examination shows periodontal inflammation with ulceration and necrosis. Laboratory results are as follows:

CBC - Hemoglobin-11.8 g/dL
Hematocrit-36%
Platelets-240,000/mm³
Leukocytes-55,000/mm³
Neutrophils-90%
Lymphocytes-8%
Monocytes-2%

This child's presentation of recurrent bacterial infections, severe periodontitis, and marked leukocytosis is consistent with leukocyte adhesion deficiency (LAD) LAD is caused by defective integrins on the leukocyte surface, which normally allow neutrophils to adhere to vascular endothelium, exit the vasculature, and migrate to areas of infection or inflammation.

Lack of neutrophil migration in LAD results in recurrent skin (eg, cellulitis, abscess, omphalitis) and mucosal (eg, periodontal) infections as well as poor wound healing. Examination shows inflammation with a notable lack of purulence. Biopsy of infected tissue is devoid of neutrophils and culture often grows Staphylococcus aureus or Gram-negative bacilli. Peripheral serum studies show marked leukocytosis and neutrophilia, particularly during episodes of infection. Classically, the first presenting sign of LAD is delayed umbilical cord separation (age >3 weeks).

(Choice A) Adenosine deaminase deficiency is an autosomal recessive form of severe combined immunodeficiency, which is characterized by deficient formation of mature B and T lymphocytes. Severe combined immunodeficiency presents with severe infections and failure to thrive. Laboratory studies show marked lymphopenia.

(Choice B) Patients with complement deficiencies are at increased risk for disseminated bacterial infections, particularly with encapsulated bacteria (eg, Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis). Cutaneous infections and neutrophilia are not seen.

(Choice C) Defective B lymphocyte maturation occurs in X-linked agammaglobulinemia (Bruton). Recurrent sinopulmonary and gastrointestinal infections with low B cell and immunoglobulin concentrations are typical. This female patient's history of periodontitis is inconsistent with X-linked agammaglobulinemia.

(Choice D) Chronic granulomatous disease (CGD) is a defect in intracellular killing due to impaired respiratory burst from activated phagocytes. Patients with CGD present with infections from catalase-positive organisms (eg, Staphylococcus aureus, Serratia marcescens, Burkholderia cepacia), Streptococcus pyogenesis catalase-negative and would be an unusual finding. In addition, patients with CGD do not have neutrophilia.

Educational objective:

Leukocyte adhesion deficiency presents with delayed umbilical cord separation, recurrent skin and mucosal bacterial infections (without purulence), and severe periodontal disease. Marked leukocytosis with neutrophil predominance is common.

A 49-year-old man comes to the emergency department with severe shortness of breath. The patient has a history of hypertension and medication nonadherence. Blood pressure is 260/144 mm Hg and pulse is 100/min. Chest examination demonstrates bibasilar crackles. There are no heart murmurs. Serum creatinine is 1.6 mg/dL. Intravenous furosemide and continuous nitroprusside infusion are started, along with noninvasive positive pressure ventilation, and he experiences improvement in his symptoms. The next morning, the patient is confused and lethargic, and he suffers a generalized tonic-clonic seizure. The skin appears flushed, and serum lactic acid level is elevated. The nitroprusside infusion rate was Kept higher !
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This patient's clinical presentation is consistent with cyanide toxicity from nitroprusside. Nitroprusside is a vasodilator with quick onset/offset kinetics commonly used for rapid blood pressure control in patients with hypertensive emergency. Nitroprusside [Na (CN),NO] rapidly decomposes to nitric oxide (NO: vasodilator) and cyanide ion (CN: toxin). Key risk factors for nitroprusside-induced cyanide toxicity include high doses, prolonged infusions, and renal insufficiency (eg, acute kidney injury due to hypertensive emergency).

Cyanide is a potent mitochondrial toxin that binds heme centers in cytochrome c oxidase (complex IV), blocking the electron transport chain. Because mitochondria are unable to reduce oxygen, venous blood returning from tissues remains saturated with oxygen and appears bright red. Loss of aerobic respiration also promotes lactic acidosis. As ATP is depleted, acute cyanide toxicity causes neurologic dysfunction (eg, altered mental status, seizures) and cardiovascular collapse.

Cyanide is cleared by rhodanese, an enzyme that transfers sulfur to cyanide to form thiocyanate (SCN) for excretion in urine. Because cyanide overdose depletes available sulfur donors, one approach to treatment is to provide additional sulfur groups with sodium thiosulfate. Other treatments include hydroxocobalamin (directly sequesters CN-) and sodium nitrite (induces methemoglobinemia to scavenge CN-).

(Choice A) Methemoglobinemia, caused by oxidizing agents (eg, nitrites, chloroquine), and carbon monoxide exposure increase hemoglobin's affinity for oxygen, which impairs oxygen unloading into the tissues. Both processes disrupt peripheral tissue oxygen delivery, leading to lactic acidosis.

(Choice B) Arsenic inhibits pyruvate dehydrogenase, the rate-limiting enzyme governing conversion of pyruvate to acetyl-CoA for entry into the tricarboxylic acid cycle, causing depletion of ATP. Acute arsenic poisoning presents with severe enteritis (diarrhea) and neurologic dysfunction

(Choice C) Ethanol is converted to acetaldehyde by alcohol dehydrogenase, with concurrent reduction of NAD+ to NADH. High NADH levels subsequently cause feedback inhibition of lactate dehydrogenase (hepatic
gluconeogenesis enzyme), leading to hypoglycemia and lactic acidosis.

Choice E) Electron transport uncouplers (eg, dinitrophenol [DNP]) cause protons to back-leak across mitochondrial membrane, dissipating the gradient as wasted heat instead of generating ATP. Because metabolic rate, these agents are occasionally abused as catabolic weight loss agents. Accidental overdose
results in fatal hyperthermia.


Take Home Point

Cyanide Toxicity an important adverse effect of nitroprusside. Blockage of ETC leads to impaired oxygen utilization, causing lactic acidosis, neurologic dysfunction, and cardiovascular collapse.

A 73-year-old man with dementia is brought to the emergency department by nursing home staff because he has been moaning continuously and gripping his lower abdomen for the past 36 hours. The patient is unable to give any history, but staff members say that he refused oral intake the previous day. He has had no vomiting or diarrhea. His last bowel movement was 2 days ago. The patient uses adult diapers, which were last changed 2 days ago. He has a history of benign prostatic hyperplasia, external hemorrhoids, hypertension, and hyperlipidemia. One year ago, he was hospitalized for diverticular bleeding that resolved spontaneously. His medications review shows that his primary care physician started amitriptyline 8 days ago for chronic neck pain. On physical examination, the patient is afebrile. His blood pressure is 160/70 mm Hg and his pulse is 100/min. The mucous membranes are moist. His lung fields are clear to auscultation. Palpation of the abdomen shows fullness and tenderness along the midline below the umbilicus without guarding or rigidity. Bowel sounds are heard in all 4 quadrants.
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This patient's clinical presentation is sufficient to initiate prompt urinary catheterization for suspected urinary retention. Bedside ultrasound or bladder scan (if available) can also help in diagnosis but should not delay urinary catheterization. Urinary catheterization can document a postvoid residual bladder volume (>50 mL is considered diagnostic for urinary retention) and provides symptomatic relief by draining urine from the distended bladder. This patient should also discontinue amitriptyline therapy.

(Choice A) An abdominal CT scan would reveal a distended bladder in this patient and may also show hydronephrosis and hydroureter However, CT scans are more expensive and time-consuming than urinary catheterization and will not provide symptomatic relief.

Choice B) Upright abdominal x-ray is not as reliable for evaluating urinary retention as it may not show a distended bladder (unless obstructed by a bladder stone). Abdominal x-rays are more useful for diagnosing ileus or small-bowel obstruction. Amitriptyline may cause ileus, but these patients typically develop nausea, vomiting, hypoactive bowel sounds, distended abdomen, diffuse mild abdominal pain, and abdominal imaging showing dilated bowel loops without air/fluid levels. This patient's normal bowel sounds, infraumbilical fullness, and lack of wet diapers for 2 days make urinary retention more likely than ileus.


(Choice C) Intravenous fluids, analgesics, and observation are the treatment for nephrolithiasis (kidney stones). Patients with kidney stones typically present with intense flank pain and hematuria instead of suprapubic fullness. Intravenous fluids could potentially worsen this patient's obstructive urinary symptoms.



Take Home Point
Drugs with anticholinergic properties can cause acute urinary retention by preventing detrusor muscle contraction and urinary sphincter relaxation. The treatment involves urinary catheterization and discontinuing the medication.

40-year-old woman is brought to the emergency department due to difficulty breathing and muscle weakness. She was one of several people who developed symptoms in a movie theater. Temperature is 36.7 C (98.1 F), blood pressure is 112/62 mm Hg, pulse is 51/min, and respirations are 24/min. On physical examination, the patient is diaphoretic. The pupils are pinpoint and unreactive, and significant tearing is noted. Diffuse rhonchi and wheezing are present in the lungs bilaterally. Muscle strength is diminished throughout, and fasciculations are noted in the extremities. First-line therapy is administered, but the patient remains weak.
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