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Chapter 74 CARDIOVASCULAR TOXICOLOGY528
BIBLIOGRAPHY
1. Antman EM, Wenger TL, Butler VP: Treatment of 150 cases of life threatening digitalis intoxication with digoxin
specific Fab antibody fragments: final report of a multi-center study. Circulation 81:1744–1752, 1990.
2. Hack JB, Lewin NA: Cardioactive steroids. In Flomenbaum NE, Goldfrank LR, Hoffman RS, et al, editors:
Goldfrank’s toxicologic emergencies, ed 8, New York, 2006, McGraw-Hill, pp 971–981.
3. Kerns W: Management of beta blocker and calcium channel antagonist toxicity. Emerg Med Clin North Am
25:309–331, 2007.
4. McCabe JL, Cobaugh DL, Menegazzi JJ, et al: Experimental tricyclic antidepressant toxicity: a randomized,
controlled comparison of hypertonic saline solution, sodium bicarbonate and hyperventilation. Ann of Emerg
Med 32(3): 329–333, 1998.
5. Wax PM: Sodium bicarbonate. In Flomenbaum NE, Goldfrank LR, Hoffman RS, et al, editors: Goldfrank’s
toxicologic emergencies, ed 8, New York, 2006, McGraw-Hill, pp 565–571.
6. Yuan TH, Kerns WP, Thomaszewski CA, et al: Insulin-glucose as adjunctive therapy for sever calcium channel
antagonist poisoning. J Toxicol Clin Toxicol 37:463–474, 1999.
ACKNOWLEDGMENT
I would like to thank Christopher DeWitt, Jody J. Rodgers, and Kennon Heard, who authored this
chapter in previous editions and contributed substantially to this edition.
529
ONE PILL CAN KILL: PEDIATRIC INGESTIONS
CHAPTER 75
Shan Yin, MD, MPH
1. What comprises the pediatric one pill can kill list?
This is a list of pharmaceuticals that may be lethal in a toddler at a therapeutic adult dose.
In actuality, the literature may not support the fact that one pill can kill. In other words, there
may not be reports of single pill ingestions causing fatalities in children. Regardless, any
ingestion by a child from this list should be considered to have the potential to produce
serious toxicity at low doses.
2. What drugs may be found on the one pill can kill list?
Although not a consensus list, these drugs are often mentioned:
n
Lomotil
n
Tricyclic antidepressants
n
Calcium channel blockers
n
b-blockers
n
Sulfonylureas
n
Clonidine
n
Camphor
n
Salicylates
n
Phenothiazines
n
Opioids
3. Describe the epidemiology of pediatric ingestions reported to U.S. poison
centers.
Approximately two thirds of ingestions reported to U.S. poison centers are pediatric, with 80%
of those occurring in children younger than 6 years of age. The epidemiology of pediatric
ingestions is bimodal, with the majority of ingestions in children younger than 6 years and
then a second smaller peak in adolescence. Children younger than 6 years are mobile and
exploratory, not having yet developed the cognitive capacity to completely understand the
potential danger of the ingestion. The increase in adolescence is largely due to self-
administration from self-harm or abuse purposes. The vast majority of pediatric ingestions
result in minimal or no clinical effects. Approximately 2% of pediatric exposures reported to
U.S. poison centers result in moderate or major outcomes or death with approximately 50%
of those in the adolescent age group.
4. What are the components of Lomotil and what are their mechanisms of
action?
Lomotil is an antidiarrheal agent composed of diphenoxylate (an opioid) and atropine
(an anticholinergic).
5. What is the presentation of a Lomotil ingestion?
Classically, Lomotil ingestions were considered to have a two-phase presentation. The first
phase consists of an anticholinergic toxidrome followed by an opiate toxidrome. This classic
presentation is unusual, and Lomotil ingestions should be considered as a long-acting opiate
ingestion, which may include features of atropine toxicity; Lomotil ingestions should be
observed for 24 hours.
Chapter 75 ONE PILL CAN KILL: PEDIATRIC INGESTIONS530
6. What is the potential lethal dose of a tricyclic antidepressant (TCA)?
The potentially lethal dose is 15 mg/kg. So in a 10-kg child, 150 mg (a one tablet adult dosing
option for amitriptyline) is potentially lethal. Doses of less than 5 mg/kg are considered to be safe.
7. What electrocardiogram (ECG) finding in TCA ingestions is helpful in
children?
The terminal 40 ms QRS axis has been shown in adults to be a useful marker in identifying
TCA overdose. In a retrospective study of 35 children presenting with TCA ingestions, the
terminal 40 ms QRS axis was not helpful in predicting TCA ingestions in children. In a study
of children and adolescents, increasing QRS duration was associated with serum tricyclic
levels, which suggested that QRS duration could be of prognostic value in a similar manner
to TCA ingestions in adults.
8. Have deaths been reported in single ingestions of dihydropyridine
(e.g., nifedipine) ingestions in children?
Yes. Although ingestions of dihydropyridines are considered to be less serious than ingestions
of phenylalkylamine (e.g., verapamil) and benzothiazepines (e.g., diltiazem) due to direct
cardiotoxicity, there is a report of a death in a 14-month-old child from a single 10-mg
ingestion of nifedipine.
9. What is the pediatric dose of calcium for calcium channel blocker ingestions?
Calcium is considered one of the first-line treatments for calcium channel blocker ingestions
and can improve inotropy and hypotension. 0.1 to 0.2 mL/kg of 10% calcium chloride or 0.3
to 0.6 mL/kg of 10% calcium gluconate can be bolused and repeated every 10 to 20 minutes
up to three to four doses. However, in severely poisoned patients, the beneficial effect of
calcium is often negligible or short-lived. Furthermore, calcium chloride can be sclerosing to
veins, an issue when dealing with the smaller-caliber veins in children. In severely poisoned
patients, it is prudent to begin other treatments such as vasopressors and inotropes
simultaneously with calcium administration.
10. What new therapy has shown some promising results in treatment of calcium
channel blockers?
Hyperinsulinemia/euglycemia has shown to be effective in animal models of calcium channel
blocker toxicity. Human case reports support improved hemodynamics with insulin/dextrose
administration, with published reports of its use in a 5-month-old child and two teenagers.
The typical suggested starting dose is 1 U/kg insulin bolus followed by a continuous infusion
of 0.5 to 1 U/kg/hr titrated to effect. Dextrose should be administered to maintain euglycemia.
11. What is a potential side effect of b-blocker ingestions other than
cardiovascular toxicity in children?
There have been reports of severe hypoglycemia associated with propranolol ingestions.
A prospective series of 208 children, however, suggested that exposure to one or two
b-blockers pills are very unlikely to result in any toxicity.
12. For how long should a sulfonylurea ingestion in a child be observed?
A child should be observed for 24 hours. There are case reports of hypoglycemia occurring up
to 21 hours after the initial ingestion. Ingestions of single tablets of glipizide have caused
hypoglycemia in children, as well as in naive adults.
13. How often should blood sugars be monitored?
Initially, blood sugars should be monitored hourly.
14. After a sulfonylurea ingestion in a child, should prophylactic dextrose or
maintenance fluids with dextrose be given?
No. Dextrose may potentiate the insulin release caused by sulfonylureas. In many reports of
delayed hypoglycemia, the child received prophylactic dextrose. The child should be allowed
Chapter 75 ONE PILL CAN KILL: PEDIATRIC INGESTIONS 531
to eat a normal diet free of concentrated sweets. If the child’s blood sugar drops, then
dextrose should be administered to bring their blood sugar up.
15. What is the rule of 50?
The rule of 50 is a mnemonic for calculating a dextrose dose for pediatric resuscitation. When
the concentration of the dextrose solution times the dose in mL/kg equals 50, 0.5 g/kg bolus
of dextrose is provided. For example, a 10% dextrose solution at 5 mL/kg or a 25% dextrose
solution at 2 mL/kg, both provide 0.5 g/kg.
16. What is considered the antidote of sulfonylurea ingestions?
Octreotide. Glucose (and sulfonylureas) opens voltage-gated calcium channels, which triggers
insulin secretion via intracellular signaling. Octreotide independently closes these channels,
resulting in decreased insulin secretion. It is important to note that octreotide does not raise
the serum blood sugar, but only stops further insulin secretion; dextrose is still needed to
normalize blood sugar when giving octreotide.
17. How is octreotide dosed in pediatric sulfonylurea ingestions?
The appropriate dose, dosing frequency, and side effect profile in pediatric sulfonylurea
ingestions has not been rigorously studied. Adults typically received 50 to 100 mg
subcutaneously every 8 to 12 hours. A suggested pediatric dose is 1 mg/kg subcutaneously
with an initial dosing interval of every 6 hours.
18. What are the cardiovascular effects that may be seen with clonidine ingestions?
Bradycardia and hypotension are most commonly reported. However, hypertension has also
been reported in children. This likely occurs from activation of peripheral a-2 receptors. The
hypertension tends to be transient and does not usually require specific treatment. Other
commonly reported effects are central nervous system (CNS) depression, respiratory
depression, hypothermia, and miosis. No specific antidote exists; treatment is generally
focused on general respiratory and hemodynamic support.
19. Can naloxone be used in pediatric clonidine ingestions?
The experience with naloxone in pediatric clonidine ingestions largely parallels the experience
with adult ingestions—it only works a fraction of the time. In a review of pediatric ingestions
receiving variable doses, naloxone was observed to have a positive response in 16% of
patients. Although clonidine ingestions often present similar to opiate ingestions, naloxone’s
effect is not completely understood.
20. How much clonidine do the 0.1 mg/day, 0.2 mg/day, and 0.3 mg/day patches
contain?
2.5 mg, 5 mg, and 7.5 mg respectively. Given that pediatric ingestions as low as 0.1 mg have
produced symptoms, ingestions of transdermal patches are particularly worrisome.
21. What are some common over-the-counter products that contain
pharmaceuticals with similar mechanisms of action to clonidine?
Oxymetazoline, naphazoline, xylometazoline, and tetrahydrozoline are imidazolines with the
same mechanism of action as clonidine. They are found in ophthalmic solutions and nasal
decongestants. Ingestion of these products can cause significant effects. As little as 2.5 to
5 mL of a 0.05% tetrahydrozoline solution caused drowsiness, bradycardia, respiratory
depression, cool extremities, and miotic pupils in a 1-year-old girl. Onset of symptoms is
typically rapid occurring in 15 to 30 minutes.
22. How do ingestions of camphor present?
Ingestions initially cause gastrointestinal symptoms such as burning of the mouth and throat
and vomiting. Severe toxicity manifests as neurologic symptoms such as seizures, hyperreflexia,
myoclonic jerks, and coma. The onset of symptoms tends to be rapid, occurring 5 to 90 minutes
following the exposure. There is no specific antidote and treatment is primarily symptomatic and
Chapter 75 ONE PILL CAN KILL: PEDIATRIC INGESTIONS532
supportive. A recent case series suggested that camphor should be considered as a cause of
undifferentiated seizures in children from communities of widespread use.
23. Where is camphor typically found?
Campho-Phenique, Vick’s Vaposteam, Vick’s VapoRub, Tiger Balm, Anbesol Cold Sore Therapy
Ointment, BenGay UltraStrength, and many other over-the-counter topical creams. The Food
and Drug Administration (FDA) has ruled that no product sold in the United States can contain
greater than 11% camphor. Foreign products, however, may contain much higher percentages
of camphor.
24. What is the potentially toxic dose of camphor?
Five hundred mg can cause serious toxicity in a child. In an 11% solution, this would equal
approximately 4.6 mL.
25. At what dose of salicylate do children begin to manifest toxicity in an acute
ingestion?
Both children and adults manifest acute toxicity at approximately 150 mg/kg. Serious toxicity
is likely to occur at 300 mg/kg.
26. How does the potency of methyl salicylate compare to salicylate?
One mg of methyl salicylate is roughly as potent as 1.4 mg of salicylate. Methyl salicylate is found
in oil of wintergreen, many topical over-the-counter creams, and many Asian herbal remedies.
27. Five mL of 100% methyl salicylate is equal to approximately how much aspirin
(or acetylsalicylate)?
Five mL (or 1 teaspoon) of 100% methyl salicylate is equal to approximately 7,000 mg of
salicylate or almost 22 regular strength adult aspirin tablets. In a 10-kg child, this would be
700 mg/kg, easily a life-threatening ingestion. Oil of wintergreen often contains 98% to
100% methyl salicylate and ingestions of 4 mL have caused death in children.
28. What phenothiazine is believed to be the most dangerous in pediatric
accidental ingestions?
Chlorpromazine (Thorazine) is responsible for nearly every serious documented pediatric
ingestion. As little as 280 mg resulted in the fatality of a 2-year-old child. An available high-
concentration chlorpromazine elixir contains 100 mg/mL. Phenothiazine toxicity manifests as
CNS depression, hypotension, and anticholinergic symptoms. Fatal pediatric cases of
neuroleptic malignant syndrome have been reported after acute ingestions of phenothiazines.
Serious morbidity or mortality has not been reported from isolated ingestions of small doses of
the antiemetic phenothiazines, promethazine (Phenergan), and prochlorperazine (Compazine).
29. What is the pathophysiology of chloroquine and hydroxychloroquine
ingestions?
These drugs are believed to exhibit quinidine-like effects and inhibit cardiac sodium and
potassium channels and may manifest with QRS prolongation, atrioventricular block,
ST- and T-wave depression, and QTc prolongation. Chloroquine is generally not found in
U.S. households because of its primary use as malarial prophylaxis or treatment. However,
hydroxychloroquine is increasingly being used as an anti-inflammatory agent. Although
hydroxychloroquine is considered safer than chloroquine, both have the potential to cause
serious toxicity including cardiotoxicity, respiratory depression, CNS depression, and seizures.
30. What other drug besides standard therapy has been used to treat chloroquine
poisoning?
Other than sodium bicarbonate for QRS widening, diazepam (2 mg/kg intravenously over
30 min) may be tried. Although its mechanism of action is unclear and randomized trials
have failed to demonstrate a clear benefit, diazepam may be considered in severe poisonings.
Chapter 75 ONE PILL CAN KILL: PEDIATRIC INGESTIONS 533
31. What newer opioid can result in significant toxicity with ingestions of
one pill?
Buprenorphine is a new opioid that is often marketed as Suboxone, contains naloxone, and is
most often used to treat opiate addiction. It is typically dosed as a dissolving sublingual tablet,
increasing the potential for toxicity in children. Ingestions of one pill have been associated
with significant respiratory depression, requiring children be observed for 24 hours after
exposure. Naloxone, used for this or any other opioid poisoning, is dosed in children
at 0.01 mg/kg intravenously for respiratory depression and 0.1 mg/kg intravenously
(up to 2 mg) for apnea.
BIBLIOGRAPHY
1. Berkovitch M, Matsui D, Fogelman R, et al: Assessment of the terminal 40-millisecond QRS vector in children
with a history of tricyclic antidepressant ingestion. Pediatr Emerg Care 11:75-77, 1995.
2. Calello DP, Osterhoudt KC, Henretig FM, et al: Octreotide for pediatric sulfonylurea overdose: review of 5 cases
[abstract]. Clin Toxicol 43: 671, 2005.
3. Clemessy JL, Angel G, Borron SW, et al: Therapeutic trial of diazepam versus placebo in acute chloroquine
intoxications of moderate gravity. Intensive Care Med 22:1400-1405, 1996.
4. Geib A, Babu K, Ewald MB, et al: Adverse effects in children after unintentional buprenorphine exposure.
Pediatrics 118:1746-1751, 2006.
5. Fiser DH, Moss MM, Walker W: Critical care for clonidine poisoning in toddlers. Crit Care Med 18:1124-1128,
1990.
6. Khine H, Weiss D, Graber N, et al: A cluster of children with seizures caused by camphor poisoning.
Pediatrics 123:1269-1272, 2009.
7. Lee DC, Greene T, Dougherty T, et al: Fatal nifedipine ingestions in children. J Emerg Med 19:359-361, 2000.
8. Love JN, Sikka N: Are 1-2 tablets dangerous? Beta-blocker exposure in toddlers. J Emerg Med 26:309-314,
2004.
9. Love JN, Smith JA, Simmons R: Are one or two dangerous? Phenothiazine exposure in toddlers. J Emerg
Med 31:53-59, 2006.
10. McCarron MA, Challoner KR, Thompson GA: Diphenoxylate-atropine (Lomotil) overdose in children: an update
(report of eight cases and review of the literature). Pediatrics 87:694-700, 1991.
11. Michael JB, Sztajnkrycer MD: Deadly pediatric poisons: nine common agents that kill at low doses. Emerg
Med Clin North Am 22: 1019–1050, 2004.
12. Quadrani DA, Spiller HA, Widder P: Five-year retrospective evaluation of sulfonylurea ingestion in children.
J Toxicol Clin Toxicol 34: 267-270, 1996.
13. Rosenbaum TG, Kou M: Are one or two dangerous? Tricyclic antidepressant exposure in toddlers. J Emerg
Med 28:169-174, 2005.
14. Shepherd G, Klein-Schwartz W: High-dose insulin therapy for calcium-channel blocker overdose.
Ann Pharmacother 39:923-930, 2005.
KEY POINTS: PEDIATRIC INGESTIONS
1. Pediatric patients can easily reach toxic doses of common medications from small amounts
of ingestions.
2. Risk of toxicity and antidote dosages are weight dependent.
3. Because specific ingested amounts are often difficult to determine in small children, prolonged
observation is often required to rule out a potentially toxic ingestion.
4. Although range of toxicity may vary, treatment for children usually mirrors that for adults
with similar ingestions.
535
PELVIC INFLAMMATORY DISEASE
CHAPTER 76
Leslie L. Armstrong, MD, and Susan Brion, MD, MS
XV. GYNECOLOGY AND OBSTETRICS
1. What is pelvic inflammatory disease (PID)?
PID represents a spectrum of disorders that are usually secondary to one or more sexually
transmitted diseases involving the upper genital tract of women. PID can include any of the
following: mucopurulent cervicitis, endometritis, salpingitis, tubo-ovarian abscess, or pelvic
peritonitis.
2. What are the risk factors for PID?
Although there are no definitive risk factors for PID, there are several likely contributors.
Age younger than 25 is seen in 75% of cases and confers 10 times the risk for the
development of PID for several reasons. Females 15 to 24 have increased number of sexual
partners, have a cervical barrier more easily breached by pathogens, often have less frequent
use of barrier contraceptives, and tend to seek health care later. Other risk factors include
earlier age at first intercourse, instrumentation including induced abortion and intrauterine
device insertion (not the IUD itself), and the period immediately following menses.
3. What are the signs and symptoms of PID?
There are no specific signs and symptoms that are diagnostic for PID. Studies have shown
that clinical diagnosis of PID may be no better than chance when compared to biopsy-proven
diagnosis. Patients present with complaints of lower abdominal pain with or without
dyspareunia, abnormal bleeding, or abnormal vaginal discharge. On examination, patients
have lower abdominal tenderness, cervical motion tenderness, and bilateral adnexal
tenderness.
4. What are the microbiologic causes?
Most cases of PID are polymicrobial. Typically, the first time a patient is diagnosed with PID it
is from a sexually transmitted disease, most commonly Neisseria gonorrhea or Chlamydia
trachomatis. Other microbials that are frequently found include pelvic anaerobes, endogenous
pelvic flora, gram-negative rods, group B strep, Mycoplasma hominis, Staphylococcus aureus,
Gardnerella vaginalis, and Haemophilus influenzae. About 15% of PID occurs in relation to
recent pelvic instrumentation (i.e., endometrial biopsy, dilation and curettage, hysterectomy,
and IUD placement).
5. What are the diagnostic criteria for PID?
Delay in diagnosis and treatment contributes to inflammatory sequelae in the upper
reproductive tract. Therefore a low threshold for the diagnosis of PID should be maintained.
The diagnosis should be considered in any female patient with a chief complaint of lower
abdominal or pelvic pain, fever, vaginal discharge, abnormal bleeding, dyspareunia, or
dysmenorrhea. Diagnostic criteria for PID present on pelvic examination include cervical
motion tenderness or uterine tenderness or adnexal tenderness. The presence of signs of
lower genital tract inflammation in addition to one of these criteria increases the specificity
of the diagnosis and empirical treatment is indicated.
Additional criteria used to support a diagnosis of PID include the following:
n
Oral temperature .38.3°C
n
Abnormal cervical or vaginal mucopurulent discharge
Chapter 76 PELVIC INFLAMMATORY DISEASE536
n
Presence of increased white blood cells on microscopy of vaginal secretions
n
Elevated erythrocyte sedimentation rate
n
Elevated C-reactive protein
n
Laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis
The most specific criteria for diagnosing PID include the following:
n
Endometrial biopsy suggesting endometritis
n
Transvaginal sonography or magnetic resonance imaging (MRI) showing thickened, fluid-
filled tubes with or without free fluid or Doppler studies showing tubal hyperemia
n
Laparoscopic abnormalities consistent with PID
6. Which diagnostic tests should be performed in patients suspected of PID?
n
A pregnancy test is necessary to rule out complications with pregnancy.
n
Ultrasound for all positive pregnancy tests to exclude ectopic pregnancy, patients being
considered for admission, or for those with a possible tubo-ovarian abscess.
n
A catheter-obtained urinalysis may reveal a urinary tract infection.
n
Cultures for C. trachomatis and N. gonorrhoeae should be obtained.
Short of laparoscopy, there is no reliable test to exclude PID. Although abnormal
laboratory results may provide supportive evidence, all laboratory studies may be normal in a
patient with PID.
7. What other diseases should be considered?
The differential diagnosis for this nonspecific presentation includes cervicitis, ectopic
pregnancy, endometriosis, ovarian cyst, ovarian torsion, spontaneous abortion, septic
abortion, cholecystitis, gastroenteritis, appendicitis, diverticulitis, pyelonephritis, and renal
colic. In a few patients, the cause of pelvic pain is never diagnosed, despite extensive testing.
8. What are the consequences of PID?
PID is associated with a number of serious clinical sequelae. Tubo-ovarian abscess is reported
in up to one third of patients hospitalized for PID. The incidence of infertility drastically
increases with each episode of PID and is thought to be primarily due to tubal occlusion from
scarring and adhesions within tubal lumens. Ectopic pregnancy risk also increases by 6- to
10-fold after an episode of PID, and the rate of a potentially fatal ectopic is 12% to 15%
higher in women who have had PID. Chronic pelvic pain may occur in up to one in three
women with PID. Fitz-Hugh-Curtis syndrome (perihepatitis) and pelvic abscess may be seen in
up to 5% to 10% of patients.
9. Who should be hospitalized?
In women with PID of mild to moderate clinical severity, outpatient therapy is reasonable. The
decision to hospitalize should be based on the severity of the patient’s presentation at the
discretion of the health care provider. However, some criteria for hospitalization are suggested
by the Centers for Disease Control and Prevention (CDC) and include the following:
n
Surgical emergencies (i.e., appendicitis) cannot be excluded
n
Pregnant patients
n
Patients who do not respond clinically to a trial of oral antimicrobial therapy
n
Patients who are unable to follow or tolerate an outpatient oral regimen
n
Patients with severe illness, nausea and vomiting, or high fever
n
Patients with tubo-ovarian abscess
10. Summarize the recommended antibiotic regimens for PID treatment.
See Table 76-1.
11. Are there alternative outpatient treatment regimens for PID?
The CDC no longer recommends fluoroquinolones for treatment of gonococcal infections
and associated conditions such as PID. Comparative evidence suggests that azithromycin
is more effective than doxycycline when given with ceftriaxone for mild PID. In a trial of
Chapter 76 PELVIC INFLAMMATORY DISEASE 537
bid, twice a day; IM; intramuscularly; IV, intravenously; PID, pelvic inflammatory disease; PO, per os; qid, four
times a day.
Recommended Oral Regimen
Ceftriaxone 250 mg IM in a single dose
Plus
Doxycycline 100 mg PO bid for 14 days
with or without
Metronidazole, 500 mg PO bid for 14 days
OR
Cefoxitin, 2 g IM, plus probenecid, 1 g PO in a single dose concurrently once; or other
parenteral third-generation cephalosporin (e.g., ceftizoxime or cefotaxime)
Plus
Doxycycline, 100 mg PO bid for 14 days
with or without Metronidazole 500 mg PO bid for 14 days
Parenteral Regimen A
Cefotetan, 2 g IV every 12 hour; or cefoxitin, 2 g IV every 6 hours
Plus
Doxycycline, 100 mg IV or PO every 12 hours
Note: Because of pain associated with infusion, doxycycline should be given orally when possible,
even when patient is hospitalized. Oral and intravenous administration of doxycycline provide
similar bioavailability. If intravenous administration is necessary, lidocaine or another short-acting
local anesthetic, heparin, or steroids with a steel needle or extension of the infusion time may
reduce infusion complications. Parenteral therapy may be discontinued 24 hours after a patient
improves clinically, and oral therapy with doxycycline (100 mg bid) should continue for 14 days.
When tubo-ovarian abscess is present, clindamycin or metronidazole may be used with doxycy-
cline for continued therapy rather than doxycycline alone because it provides more effective
anaerobic coverage.
Parenteral Regimen B
Clindamycin, 900 mg IV every 8 hours
Plus
Gentamicin, loading dose IV or IM (2 mg/kg body weight), followed by a maintenance dose
(1.5 mg/kg) every 8 hours. Single daily dosing may be substituted.
Note: Although use of one daily dose of gentamicin has not been evaluated for the treatment of
PID, it is efficacious in analogous situations. Parenteral therapy may be discontinued 24 hours
after a patient improves clinically, and continuing oral therapy should consist of doxycycline,
100 mg PO bid, or clindamycin, 450 mg PO qid, to complete 14 days of therapy. When
tubo-ovarian abscess is present, clindamycin may be used for continued therapy rather than
doxycycline because clindamycin provides more effective anaerobic coverage.
TABLE 76-1. OUTPATIENT TREATMENT OF PELVIC INFLAMMATORY DISEASE
Adapted from Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines.
MMWR Morb Mortal Wkly Rep 56 (14):332, 2007.