Senior Report 8.11

seniorreport

Case Presentation by Alex Weissman, MD

Chief Complaint: “I feel terrible.”

History of Presenting Illness:
The patient is a 32-year-old female presenting with complaint of feeling “terrible and weak.” She states that this has happened to her twice in the last 24 hours. The first episode occurred upon awakening at 3 AM this morning with a sensation of doom, shortness of breath, chest pain, and in a cold sweat with chills. Subsequently she passed out. She ate some corn, felt better, and went back to sleep. Today, prior to arrival, the patient had another episode where she went into a cold sweat with chills and had a sensation of doom with chest pain and shortness of breath; however, this time she did not pass out. She called EMS, who found her capillary blood sugar was 32 mg/dL. The patient denies being sick recently. She denies insulin or sulfonylurea use. She denies abnormal stress in her life. She states that she has been eating normally. Last menstrual period was 3 years ago, the patient has always had irregular menses. The patient denies associated headache, sudden change in vision, abdominal pain, nausea, vomiting, diarrhea, constipation, dysuria, pain or numbness in the extremities, recent illness, or recent travel.

Review of System:
Constitutional: Complains of cold sweats and chills
HEENT: Denies headache
CVS: Complains of substernal chest pain
Lungs: Complains of SOB
Abdomen: Denies abdominal pain
Musculoskeletal: Denies pain in the extremities
Genitourinary: Denies dysuria
Skin: Denies rash
Neurologic: Denies numbness
Psychiatric: Denies depression

 

Past Medical History:
Bronchitis, splenomegaly, anemia, thrombocytopenia

Past Surgical History:
Bone marrow biopsy

Social History:
The patient denies use of tobacco, alcohol, or illicit drugs past or present.

Family Medical History:
Addison’s disease in her mother

Physical Exam:
Vitals: Blood pressure: 100/75, Pulse: 60, Respiratory rate: 18, Pulse Oximetry: Not initially recorded, Temperature: 36.2 degrees Celsius
General: Alert and oriented x3, no acute respiratory distress
Head: normocephalic, atraumatic
Eyes: PERRL, EOMI, bilateral conjunctival pallor, no scleral icterus
ENT: No cervical lymphadenopathy, no pharyngeal edema, mucous membranes moist
Cardiovascular: regular rate and rhythm, no appreciable murmurs, capillary refill <2 seconds
Respiratory: no tachypnea, no retractions, clear to ausculation bilaterally, no appreciable wheezes, rhonchi, or rales
Gastrointestinal: normoactive bowel sounds, nondistended, no tympany to percussion, soft and nontender to palpation
Musculoskeletal: Extremities are atraumatic, dorsalis pedis and radial pulses 2+ and regular bilaterally, no peripheral edema
Skin: no rashes or lesions
Neurological:
MENTAL STATUS: awake, alert, oriented
CRANIAL NERVES: face symmetric, pupils 3mm -> 2mm bilaterally, PERRL, EOMI, visual fields full to confrontation
MOTOR: patient moving all four extremities spontaneously, gait normal
SENSORY: intact to light touch

ECG:
Alex

 

Labs:

Initial CBG – 32 mg/dL

Electrolytes:

132 99 13 9.3 51
5.2 22 0.46 2.1

TSH: 3.586 Micro IU/mL

CBC:

4.7 11.1 109
33.3

Serum pregnancy: negative
Insulin: <0.5 mcUnits/mL
Random cortisol: 2.2 mcg/dL

 

Questions:

1) What are the classic physical exam and laboratory findings in primary adrenal insufficiency (Addison’s Disease)?
a) High blood pressure, high serum potassium, high serum sodium, low random cortisol, low serum glucose
b) Low blood pressure, high serum potassium, low serum sodium, low random cortisol, low serum glucose
c) High blood pressure, high serum potassium, low serum sodium, high random cortisol, high serum glucose
d) Low blood pressure, low serum potassium, low serum sodium, low random cortisol, low serum glucose

2) What laboratory test is used to diagnose adrenal insufficiency, what distinguishes primary versus secondary adrenal insufficiency, and what test value would you expect in primary adrenal insufficiency?
a) ACTH stimulating test; ACTH; low or normal ACTH level
b) Random cortisol; cortisol; low cortisol
c) ACTH stimulating test; ACTH; high ACTH level
d) Random cortisol; ACTH; low or normal ACTH level

3) What are some basic differences in symptomatology between primary and secondary adrenal deficiency?
a) Primary: Hypokalemia, hypernatremia, hypoglycemia, dehydration, hypotension, Cushingoid habitus
Secondary: Hyperkalemia, hyponatremia, normotension, hyperpigmentation, hyperglycemia

b) Primary: Hyperkalemia, hyponatremia, hypoglycemia, dehydration, hypotension, hyperpigmentation,
Secondary: Hypokalemia, hyper/hyponatremia, +/- Cushingoid habitus, hypoglycemia

c) Primary: Hypokalemia, hyponatremia, dehydration, hypotension, +/- Cushingoid habitus, hyperglycemia
Secondary: Hypernatremia, hyperkalemia, hyperpigmentation, normotension
d) Primary: Hyperkalemia, hyponatremia, hyperglycemia, normotension
Secondary: Hypokalemia, hypernatremia, hypoglycemia, hypotension, dehydration, hyperpigmentation, +/- Cushingoid     habitus

 

Bonus Question 1. What is the preferred steroid treatment for adrenal crisis and what vital sign abnormality should raise the ED physician’s clinical suspicion for an adrenal crisis?
a) Hydrocortisone – unexplained hypotension
b) Prednisone – unexplained hypertension
c) Dexamethasone – unexplained hypotension
d) Hydrocortisone – unexplained hypertension

 

Bonus question 2: What is the most common infectious cause of primary adrenal insufficiency in the US?
a) Tuberculosis
b) Meningitis
c) Influenza
d) HIV

Answers & Discussion:

1) Correct answer: B
Primary adrenal insufficiency is characterized by failure of the adrenal gland to produce sufficient steroids including glucocorticoids (namely cortisol), mineralocorticoids (namely aldosterone), and gonadocorticoids (namely estrogen and testosterone). It can be associated with infectious disease states (HIV, tuberculosis, adrenal hemorrhage, sepsis), autoimmunity (polyglandular autoimmune syndrome type I or II), inflammatory diseases (sarcoidosis, hemochromatosis, amyloidosis, lymphoma, etc.), congenital/hereditary causes (congenital adrenal hyperplasia, adrenal hypoplasia, adrenal leukodystrophy, familial glucocorticoid deficiency), or secondary to non-steroid drugs (ketoconazole, mitotane, aminoglutethimide, hemorrhage from warfarin, prolonged IV infusions of etomidate, etc.). It often presents with a shock state due to the body’s inability to produce the stress hormone, cortisol, as well as the lack of aldosterone. Patients typically have low blood pressure, low glucose, low serum sodium, low cortisol levels, and high serum potassium. A random cortisol level less than 3 mcg/dL is diagnostic. The low blood pressure, low serum sodium, and high serum potassium are related to decreased aldosterone levels that are secondary to the adrenal gland failure. Decreased cortisol also leads to decreased blood pressure as well as decreased glucose. Vague GI complaints, salt craving, and postural syncope are common complaints. Another result of adrenal insufficiency is decreased estrogen and testosterone levels.

Secondary adrenal insufficiency occurs when there is failure of the hypothalamus-pituitary-adrenal axis typically at the level of the hypothalamus or pituitary gland, instead of singular failure of the adrenal gland as seen in primary adrenal insufficiency. It is most commonly is due to abrupt withdrawal of long-term high dose steroids. Only cortisol will be low, as opposed to low cortisol and low aldosterone in primary adrenal insufficiency. Other causes of secondary adrenal insufficiency are Sheehan syndrome, head trauma, pituitary disease, infectious diseases affecting the hypothalamus or pituitary (tuberculosis, HIV, meningitis, etc.), or inflammatory diseases affecting the hypothalamus or pituitary (sarcoidosis, cancer, hemochromatosis, etc.).

2) Correct answer: C
Recall that the hypothalamus secretes corticotropin-releasing factor that causes the pituitary to release ACTH, thus resulting in the adrenal gland secreting cortisol. Therefore, the rapid cosyntropin (synthetic ACTH) stimulation test is utilized to diagnose adrenal insufficiency, and the level of plasma ACTH is used to distinguish between primary (a.k.a. adrenal gland failure) and secondary (a.k.a. hypothalamus or pituitary failure) adrenal insufficiency. The cosyntropin test is performed by drawing a baseline cortisol level (18-20 mcg/dL is a normal random cortisol in healthy people), then administering 0.25 mg IV ACTH, and checking plasma cortisol at 30 minutes and 1 hour after administration. In normal people, the plasma cortisol should rise by at least 7 mcg/dL at 30 minutes and peak at >18 mcg/dL at 1 hour.    A high ACTH level is indicative of primary adrenal insufficiency, hence the adrenal glands are not producing sufficient cortisol despite the hypothalamus and pituitary telling them to do so. Since there is no feedback inhibition from circulating cortisol, more and more ACTH is released. A low or normal ACTH level is suggestive of secondary adrenal insufficiency, indicating a problem at the level of the hypothalamus or pituitary gland.

3) Correct answer: B
Primary adrenal insufficiency is characterized by both aldosterone deficiency and cortisol deficiency. Aldosterone deficiency confers hypotension and hyponatremia with hyperkalemia. Cortisol deficiency confers weakness, lethargy, hypotension, hyperpigmentation (due to unopposed ACTH production) and hypoglycemia.

Secondary adrenal insufficiency has intact aldosterone presence, therefore unless the patient is in an adrenal crisis, blood pressure is typically normal. Hypernatremia can result since aldosterone function is intact, unless there is a dilutional hyponatremia secondary to retained water. Hypokalemia results from the unchecked aldosterone effect. There is often hypoglycemia secondary to the lack of ACTH stimulation on cortisol release.

EKG changes can occur secondary to the potassium disturbances: U waves from hypokalemia, or peaked T waves with QT prolongation or even heart block can occur due to hyperkalemia.

Bonus 1: Correct answer: A
High dose steroid administration is the mainstay of therapy for adrenal crisis, regardless of cause or level of dysfunction in the hypothalamic-pituitary-adrenal axis, in addition to supportive care and treatment of the underlying etiology. Hydrocortisone 100 mg IV is the preferred steroid because it has both mineralocorticoid and glucocorticoid effects. If an ACTH stimulating test is going to be ordered, then Dexamethasone 4 mg IV can be used instead because it does not interfere with the test results. Prednisone is not strong enough for a patient with an adrenal crisis. Unexplained hypotension should increase the clinician’s suspicion for an adrenal pathology, especially hypotension refractory to fluids and vasopressors. This occurs secondary to the lack of cortisol. Of course, fluids (dextrose 5% with 0.9% normal saline or hypertonic saline if needed) and vasopressors (norepinephrine, dopamine, or phenylephrine) should absolutely be given in addition to steroids during an adrenal crisis.

Bonus 2 Correct answer: D
HIV (and especially HIV related infections) is the most common cause of primary adrenal insufficiency in the US, but worldwide the most common cause is tuberculosis.

References:

  1. Tintinalli, Judith E, et al. Tintinalli’s Emergency Medicine, 7th Ed. San Francisco: McGraw-Hill, 2011. Print. Chapter 225: Adrenal Insufficiency and Adrenal Crisis, 1453-1456.
  1. Marx, John A, et al. Rosen’s Emergency Medicine, 7th Ed. Philadelphia: Mosby Elsevier, 2010. Print. Chapter 126: Thyroid and Adrenal Disorders, 1671-1675.

Intern Report 8.10

internreport

Case Presentation by Amy Buth, MD

A 12 y/o G0P0 presents to the ED with her mother and grandfather with complaints of vaginal bleeding for the past 20 days. Four days prior, she developed a severe frontal headache with fatigue. This morning she felt nauseated and had one episode of nonbloody/nonbilious emesis. She also developed diffuse abdominal cramps with extreme fatigue, leading to her collapsing at home. Her mother therefore brought her daughter in to the ED right away. Per the mother, the patient has irregular heavy periods which last 7 -10 days. Menarche was December 2013. Last cycle was October 14-November 4, 2014. She missed her cycle in August and September of 2014. During the past 20 days, she has been using 10 pads/day and noticing clots. She is not sexually active and denies any trauma or abuse. She currently feels weak and dizzy. She denies any fevers, chills, chest pain, shortness of breath, dysuria, hematuria, increased urgency or frequency with urination, or diarrhea.

PAST HISTORY:
PMH: Asthma (resolved)
SurgH: Right inguinal hernia repair 2011
Gyn: G0P0. Began menstruating December 2013; typically as a 7 day cycle
Meds: Tylenol for pain PRN
Allergies: none
FH: Denies family history of bleeding, bruising, thrombotic disease, breast/uterine/ovarian/colon cancer, hypertension, or diabetes
SH: denies alcohol, tobacco, illicit drug use. The patient is a Jehovah Witness

PHYSICAL EXAMINATION:

Vitals: Temp 37.0 oral, BP 120/66, HR 118, RR 20, 98% on RA. Positive orthostatics

Constitutional: Lethargic, poor eye contact, laying on the bed in mild distress.

Eye: PERRL, EOMI, no discharge, conjunctival pallor

Respiratory: Lungs CTA bilaterally, no cough, no wheezing, no cyanosis.

Cardiovascular: Tachycardia, regular rhythm, no chest pain, no palpitations, no peripheral edema, good pulses equal in all extremities

Gastrointestinal: Bilateral lower quadrant tenderness, no distension, no rebound tenderness, no palpable masses

Genitourinary: Pelvic exam: normal external genitalia, blood at the introitus, blood noted in the vaginal vault, there is slow active bleeding from the cervix. Bimanual exam: uterus is anteverted and normal in size, no adnexal masses or tenderness, no cervical motion tenderness

Integumentary: Warm, dry, pallor

Hematology/Lymphatics: No petechia or bruising

Neurologic: Symmetric face, decreased strength in all extremities bilaterally secondary to fatigue and poor effort

LABORATORY STUDIES:

Pregnancy test: negative

CBC: 6.8>4.6/14.7<393 with 77% PMNs and 19% lymphs. MCV 75 and RDW 13.6

BMP: 137/3.8/103/24/11/0.52, glucose 98

Lactate 2.8

PT/PTT/INR: 11.4/21.5/1.07

TSH 6.149 (NL 0.210 – 4.940), T3 total 139 (NL 60 – 180), T3 free 3.9 (NL 1.4 – 4.4), total Thyroxine 8.7 (NL 6.2 – 14.6), free Thyroxine 1.1 (NL 0.8 – 1.8)

Prolactin 15.3 (NL 2.8 – 29.2)

von Willebrand activity 348 (NL 43-138), von Willebrand antigen 244 (60-153), Factor VIII 395.7 (63-150)

Questions:

1) What is the patient’s most likely diagnosis?
a) Leiomyoma
b) Hypothyroidism
c) Anovulatory bleeding
d) von Willebrand Disease

2) After placing the patient on a cardiac monitor and starting a fluid bolus, what would be the best next step?
a) Uterine packing
b) Order O negative blood
c) Order a stat transvaginal ultrasound
d) Consult pediatric gynecology

3) What is the typical treatment for this diagnosis?
a) Gonadotropin-releasing hormone agonists
b) Synthetic thyroid hormone therapy
c) High dose estrogen therapy
d) Desmopressin / DDAVP

4) BONUS: The patient and her family are Jehova’s Witnesses. You develop great rapport with the family and have a heart to heart discussion about the patient’s treatment and safety. The patient and her family are grateful for your recommendations but are refusing a blood transfusion. They are agreeable to discuss alternative treatment plans. The patient is tachycardic, lethargic, orthostatic, and actively bleeding with Hg 4.7. You again strongly encourage the importance of the blood transfusion. The family then asks to be discharged so they can go to another Children’s Hospital that has a Jehovah’s witness liaison for more direction. What do you do?
a) Follow the patient/family’s wishes and do not give a blood transfusion. Consider other options.
b) Discharge the patient so they can go to another facility of their choice
c) Contact the court to make a ruling
d) Call security to keep the patient and proceed to give the blood transfusion

Answers:
1. C
2. B
3. C
4. D

 

8.10

Question 1: Perimenarchal adolescents who have abnormal uterine bleeding typically results from anovulation (C). During the anovulatory cycle, estrogen levels rise but in the absence of ovulation, a corpus luteum never forms. Therefore, progesterone is not produced, causing the endometrium to become hyperproliferative. Once the endometrium outgrows its estrogen supply, it leads to irregular sloughing and bleeding. Sometimes anovulation occurs from an abnormality in the hypothalamic-pituitary-ovarian axis. The hypothalamus secretes GnRH which stimulates the pituitary to produce FSH and LH which act on the ovarian follicles and ovarian theca cells respectively. If there is an alteration to the GnRH release, this will affect FSH and LH. Thus, if there is a decrease in GnRH such as with hypothyroidism (C), this leads to decreased FSH/LH that may result in amenorrhea. Increased prolactin can also lead to GnRH suppression and amenorrhea. Hyperthyroidism on the other hand would lead to menorrhagia. In this case, the patient had an elevated TSH but normal T3/T4 results which suggests subclinical hypothyroidism which would not cause the irregular heavy bleeding. She also had a normal prolactin level. Polyps, leiomyomas (A), and ovarian neoplasms leading to irregular bleeding are less frequent in this young adolescent group. If there is considerable bleeding around menarche enough to necessitate blood transfusions, coagulopathies like von Willebrand Disease (D) should be excluded. VWD is a common coagulation abnormality that arises from a deficiency of von Willebrand factor, a protein required for platelet adhesion, platelet-endothelial adhesion, and fibrin clot formation by acting as a carrier protein for factor VIII. In this patient, the von Willebrand activity (also known as the Ristocetin Cofactor) is elevated to 348 (normal 43-138), von Willebrand antigen is elevated at 244 (normal 60-153), and factor VIII is 395.7 (normal 63-150). Patients with VWD typically have normal to decreased levels of VWF antigen, VWF activity, and Factor VIII. A possible explanation for the elevated levels is that VWF is an acute phase reactant that could be elevated secondary to the patient’s clinical state.

Question 2: After running through ABCs and beginning fluid resuscitation, the patient should receive a blood transfusion (B) due to her Hg being 4.6 with tachycardia, lethargy, lightheadedness, fatigue, and positive orthostatics. This patient is symptomatic from her anemia secondary to vaginal bleeding. She is actively bleeding but not profusely bleeding due to a ruptured major vessel. Uterine packing (A) may be necessary in severe life-threatening blood loss. Specifically, a foley catheter can be placed in the cervix to tamponade the bleeding. Packing in light bleeding has increased risk of infection and is usually avoided. A transvaginal ultrasound (C) is needed, but should wait until the patient is stable for imaging. Pediatric gynecology (D) should be consulted but the patient is unstable and needs blood products first.

Question 3: The treatment for anovulatory bleeding in this patient is high dose estrogen therapy which should be initiated after OBGYN consultation and recommendations (C). If Hg >12 g/dL you can supplement with iron, NSAIDS to help reduce flow, and consider oral contraceptive pills if the patient is sexually active. If Hg 9-12 g/dL, OCP BID until bleeding stops and continue OCP QD for 21 days followed by 1 week of placebo pills. If Hg <9 g/dL, admit to hospital and transfuse based on degree of hemodynamic instability. OCP Q4H until bleeding slows and then OCP QID for 2-4 days followed by OCP TID for 3 days, and then OCP BID for total of 21 days or until HCT >30%. Gonadotropin-releasing hormone agonists (A) can be used for temporarily shrinking uterine fibroids and temporarily stop menstrual bleeding. Hormonal birth control can also be used to reduce bleeding, cramps, and pain for women with fibroids. Synthetic thyroid hormone therapy (B) is used for hypothyroidism. Desmopressin / DDAVP (D) is used for von Willebrand Disease. It is known to increase VWF and factor VIII levels.

Question 4: This is a tricky ethical question because the patient herself is refusing blood as well as her parents. She is a minor and cannot make decisions on her own at this point. In general, if a child needs blood to save his/her life, you must give blood (D) – even over the objection of the patient and parents. Parents do not have the right to refuse life saving treatment for a minor. It is important though to seek parental consent for their child even if they refuse. This may lead to a constructive conversation that could provide the family with a better understanding of why the patient needs the blood transfusion. In this particular case, the blood products were ordered, and the ED physicians and the family had a long conversation about the benefits and risks of the transfusion. The family kept refusing the transfusion. Hematology was consulted to see if there was any other option to treat the anemia. They said blood was necessary. Therefore, two services and two ED physicians were in agreement to the blood transfusion. By this time, the blood arrived, and the family tried to leave AMA. The ED physicians called a member of the ethics committee who agreed the patient’s safety takes over and a blood transfusion was necessary. Fortunately, good rapport was eventually made between the family and the physicians, and the family finally signed consent for a unit of packed red blood cells. OBGYN was involved and initiated Premarin.

 

REFERENCES:
Hoffman BL et al. Chapter 8. Abnormal Uterine Bleeding. Williams Gynecology, 2eNew York, NY: McGraw-Hill; 2012.

Morrison LJ, Spence JM. Chapter 99. Vaginal Bleeding in the Nonpregnant Patient.  Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e.New York, NY: McGraw-Hill; 2011.

Rick, Margaret. Treatment of von Willebrand disease. UptoDate. Nov 1, 2013

Sass AE, Kaplan DW. Adolescence.  CURRENT Diagnosis & Treatment: Pediatrics, 22eNew York, NY: McGraw-Hill; 2013.

Stewart, Elizabeth. Uterine Fibroids: Beyond the Basics. UpToDate. Oct 11, 2013

Image courtesy of ScienceBlogs: Pharyngula. http://scienceblogs.com/pharyngula/2006/04/06/why-the-wingnuts-hate-plan-b/.

Intern Report 8.9

internreport

Case Presentation by Devina Mohan, MD

Chief Complaint: “I’ve been feeling bad for one week”

HPI: 56-year-old female with PMH of diabetes and hypertension comes to the ED complaining of feeling bad for the past week. She states that it all started after she was cleaning her basement after the flood last week. Initially she just feeling sick and in the past 2-3 days she has had cough with productive white sputum and subjective fevers. She states that she has not taken anything for her symptoms. She states her children were concerned about her today and sent her in. Patient denies sore throat, congestion, numbness or weakness in extremities, dysuria, hematuria, blood in stool, diarrhea, constipation.

PMH: hypertension, diabetes
PSH: cholecystectomy, small bowel resection, umbilical hernia repair
MEDS: Humulin 70/30, Quinapril 40 mg, Chlorthalidone 25 mg
ALLERGIES: Penicillin
SH: Denies tobacco, alcohol, or drug use
FH: Hypertension

EXAMINATION OF ORGAN SYSTEMS/BODY AREAS:
Vitals: BP 82/54, HR 137, RR 18, temp 39.8, O2 sat 100% on RA
Cardiovascular: Tachycardic rate with normal rhythm, no murmurs
Respiratory: Diminished breath sounds on left lower lobe, no wheezing, no crackles
Gastrointestinal: Soft, +BS, non-distended, mildly tender to palpation diffusely, no rebound, no guarding
Musculoskeletal: No obvious deformities, 2+ bilateral radial and DP pulses, good capillary refill
Skin: Skin is cool to the touch but good capillary refill, no rashes
Neurological: AOx3, moving all 4 extremities, gait not observed as patient is feeling too weak to stand

 

CXR:
8.9

CBC
WBC – 14.6
Hgb – 13.7
Platelets – 116

BMP
Na – 127
K – 3.9
Cl – 90
CO2 – 18
BUN – 31
Cr – 3.41
Glucose – 454

Troponin – 0.272

 Questions:

1. Given the above data, which would be the best diagnosis and disposition for this patient?

a) Community acquired pneumonia – oral levofloxacin, discharge home
b) Community acquired pneumonia – ceftriaxone and azithromycin, admit to medicine
c) Community acquired pneumonia – cefepime and azithromycin, admit to ICU
d) Healthcare associated pneumonia – vancomycin and levofloxacin, admit to ICU

2. What is the patient’s CURB65 score?
a) 1
b) 2
c) 3
d) 4

3. What additional test is indicated to best treat this patient?
a) CT Chest
b) ABG
c) RSV swab
d) Urine legionella antigen

Answers & Discussion
1) C
2) B
3) D

1) C
The patient has a community acquired pneumonia. Based on the fact that she is hypotensive and seems to have acute end-organ dysfunction with elevated creatinine and troponin, the patient does require admission. The antibiotic guidelines in the DMC system at this time for a CAP requiring admission to the floors are ceftriaxone 1g IV q12 and doxycycline PO 100mg q12. Azithromycin 500mg PO q24h can be substituted for doxycycline if not tolerated.

Given her hypotension & tachycardia, patient would require ICU admission if she did not improve with treatment.  Based upon and ICU admission she should be given cefepime and azithromycin.

Community acquired pneumonias (CAP) are acute infections obtained in the community and distinguished from the HCAP and HAP as below. Most common pathogens are S. pneumoniae, Mycoplasma pneumoniae, Chlamydophila pneumoniae and respiratory viruses. Treatment guidelines usually based on resistance to S. pneumoniae. Coverage of atypical pathogens in the outpatient setting is usually unnecessary as they are usually self-limiting and affect younger persons.

  • Widespread use of fluoroquinolone in outpatient setting is discouraged due to concern for development of resistance and colonization. Recommendations based on IDSA and BTS:
  • Outpatient (patient with no comorbidities, recent abx use, or high rates of resistance): Doxycycline
  • Outpatient (patient with comorbidities, use of abx within prior 3 months): Levofloxacin OR combination of beta-lactam (amoxicillin, amoxicillin and clavulanate potassium, ceftriaxone, cefuroxime) and azithromycin
  • Hospitalized patient (medicine): Levofloxacin OR combination of beta-lactam (cefotaxime, ceftriaxone, amoxicillin and clavulanate potassium) plus azithromycin
  • Hospitalized patient (ICU): combination of beta-lactam (cefotaxime, ceftriaxone, amoxicillin and clavulanate potassium) plus azithromycin OR combination of beta-lactam (cefotaxime, ceftriaxone, amoxicillin and clavulanate potassium) plus fluoroquinolone

Healthcare-associated pneumonia (HCAP) is pneumonia occurring in a non-hospitalized patient with extensive healthcare contract. This includes IV therapy, wound care, chemotherapy within 30 days of illness. Also, residence in a nursing home or other long-term care facility, admission in a hospital for 2 or more days within the prior 90 days, and attendance at a hospital or dialysis center within prior 30 days.

Hospital-acquired pneumonia (HAP) is pneumonia occurring 48 hours or more after admission and did not appear to be incubating at the time of admission.

Ventilator-associated pneumonia is a type of HAP that develops more than 48-72 hours after intubation.

  • Treatment for HCAP, HAP, and VAP all tend to be based on the institutions resistance patterns and risk factors for multidrug resistance in the patients. These include recent antibiotic use.
  • Important to culture and target therapy once susceptibilities are identified
  • Add anti-pseudomonal coverage if it is a concern (piperacillin and tazobactam, cefepime, meropenem)
  • Add MRSA coverage if that is a concern (vancomycin, linezolid)
  • DMC pharmacy guidelines
    • HCAP (medicine admit): cefepime plus doxycycline plus vancomycin
    • HCAP (ICU admit): cefepime plus vancomycin plus azithromycin plus tobramycin
    • HAP/VAP: cefepime plus vancomycin plus tobramycin
    • HAP/VAP (with exposure to piperacillin and tazobactam or cefepime within prior 90 days): meropenem plus vancomycin plus tobramycin

2) B
The patient in the question had a CURB65 score of 2, with recommendation to hospitalize.

 CURB 65 is a clinical prediction rule based on five factors to predict 30-day mortality. The five factors are presence of confusion, BUN>7 mmol/L, respiratory rate>30 breaths/min, BP (systolic <90mmHg, diastolic <60mmHg), age >65.

  • 0 points: 0.7%, recommend treat as outpatient
  • 1 point: 2.1%, recommend treat as outpatient
  • 2 points: 9.2%, recommend admission to hospital
  • 3 points: 14.5%, recommend admission, consider ICU
  • 4 or 5 points: 40%, recommend ICU admission

The Pneumonia Severity Index (PSI) is another clinical prediction rule that has been validated and is widely endorsed. However, it involves a multistep process and classifies patients into risk classes II-V based on a point system from under 70 to over 130. Factors included are comorbidities such as neoplastic disease, heart disease, renal disease, etc; age, vital signs and mental status, and various lab findings. It is a lot more complex and maybe not as fast and efficient. The limitations of the PSI are that it underestimates severity, especially in young patients without comorbidities.

Limitations of the CURB 65 are that it may underestimate risk in elderly patients with co-morbidities.

3) D
Legionella pneumophila habituate in aquatic bodies, such as lakes and streams. Water distribution systems amplify the proliferation of the organism. The presence of algae, amebae and other bacteria also promote growth. There has been a link to aspiration of contaminated water and rainfall. The patient in the question was exposed to a lot of stagnant water while cleaning her flooded basement. A urine legionella antigen was obtained and turned out to be positive.

A CT chest could be useful if the patient had recurrent pneumonias in the same spot to identify any anatomic abnormalities or malignant lesions causing obstruction and proliferation of bacteria in one particular lobe. In this situation, we have no history of a recurrent pneumonia to necessitate a CT scan.

An ABG would be useful to evaluate hypoxemia and acidosis. The patient does have a level of acidosis based on her BMP and will likely need an ABG. However, in the initial phases of treatment, it would not change management drastically. The patient will still need resuscitation and antibiotics.

The patient would additionally require further follow up of the elevated troponins, cardiac surveillance, blood cultures and tailoring of therapy based on findings.