Nightingale’s Numbers

As we prepare to celebrate nurses in the month of May, I’m reflecting on the famous Florence Nightingale. Among the many accomplishments attributed to “the lady with the lamp,” perhaps the least celebrated, but arguably most impactful, was her pioneering use of storytelling through statistics. She collected data and computed equations like a mathematician but added the human element like only a nurse could. She and her team produced visually impactful data demonstrating that during the Crimean War, more soldiers were dying from preventable complications than from wounds sustained in battle.1 Her tireless work to relay those numbers in terms of human lives is what convinced those in power to invest in necessary improvements.Sometimes nursing documentation, medical record audits, and data collection for quality improvement seem mundane compared with the physical work of caring for patients. It is good to remember that even Florence put in the time to do this work, knowing that in this way the nurse cares not only for patients in the beds but also for future patients yet to fall ill. Confusion and restlessness are early indicators of hypoxemia, especially in older adults. When fluid rapidly shifts into the alveoli, gas exchange is impaired, decreasing oxygenation of the brain. The mental status change will happen before other vital signs change and may indicate decreased levels of oxygen in the blood, raising concern for cardiogenic shock. Oliguria reflects poor renal perfusion, but urine output of 30 mL/h is still within normal limits (A). Edema of the lower extremities and abdominal firmness may indicate worsening heart failure but not necessarily cardiogenic shock (C). Although hypotension may indicate impending shock, the cutoff systolic blood pressure for a cardiogenic shock definition is less than 90 mm Hg (D) and the mental status change is more concerning. Conduction delays should be treated with permanent pacemaker implantation when the cause is determined to be irreversible. Prinzmetal angina, also known as vasospastic angina, is often treatable, and a resulting conduction delay would not usually be permanent (A). Endocarditis would be treated with antibiotics, and resulting conduction delays may be reversible (B). Conduction delays are a known complication of transcatheter aortic valve replacement, but patients who have undergone this procedure are usually monitored for a minimum of 24 hours before the decision is made to implant a permanent pacemaker (C). Air trapping and lung hyperinflation are complications of asthma exacerbation. For patients requiring mechanical ventilation, an inspiratory to expiratory ratio of 1:4 to 1:5 is best to allow sufficient time for exhalation. The best way to accomplish this ratio on the ventilator is to set a slow respiratory rate of 12/min to 14/min (C). Asthma exacerbation is characterized by auto-PEEP, a condition in which the lungs retain excess air and pressure at the end of an exhalation. Setting extrinsic PEEP on the ventilator may be harmful (B). Tidal volumes should be set low to treat asthma, with the ideal between 6 and 8 mL/kg body weight (D). Assessment data that indicate hyperglycemic hyperosmolar state include severe dehydration and electrolyte loss, which would lead to dry mucous membranes. Kussmaul respirations (A) are very deep breaths that are driven by the body’s attempt to regulate pH in patients with diabetic ketoacidosis. Ketone breath odor and nausea (C), as well as diarrhea and epigastric pain (D), are also findings in patients with diabetic ketoacidosis. Widening pulse pressure, bradycardia, and irregular respirations are elements of the Cushing triad, which indicates rising intracranial pressure and impending brain herniation. An increased respiratory rate and tachycardia may indicate distress, pain, or a shock response but not impending herniation (A). The Battle sign (bruising behind the ear) and leakage of fluid from the ear may indicate a basilar skull fracture but not rising intracranial pressure and herniation (B). Sluggish bilateral pupillary response may indicate a neuropathology, but 1-sided pupil dilation is more indicative of rising intracranial pressure (D). The child is presumably experiencing symptomatic hyponatremia, as evidenced by seizure activity, postictal somnolence, and a critically low serum sodium level. The most appropriate immediate intervention is administration of intravenous hypertonic saline, specifically 3% sodium chloride at 3 mL/kg over 15 minutes, to raise the sodium level to prevent further cerebral edema and neurologic deterioration. Furosemide (A) promotes free water excretion but does not correct the potentially life-threatening hyponatremia and could worsen the acute condition. Administering isotonic saline (C) is appropriate in patients with gradual or less severe hyponatremia but is insufficient for urgent correction when neurologic symptoms are already present. Similarly, simply reducing the fluid rate (D) will not correct the low sodium level in a timely manner and would place the child at risk for worsening cerebral complications. The presentation is consistent with multisystem inflammatory syndrome in children. The anticipated next intervention is intravenous immunoglobulin, which is the first-line therapy to modulate the hyperinflammatory response and reduce the risk of cardiovascular complications. An urgent abdominal computed tomography scan is not immediately indicated unless there is evidence of acute abdominal pathology, and this scan does not address the systemic inflammatory condition (B). Continuous renal replacement therapy is not warranted without renal failure or significant fluid overload (C). A norepinephrine infusion may support blood pressure if shock develops, but it does not treat the underlying immune dysregulation driving the patient’s illness (D). The child presents with hypoperfusion, as evidenced by hypotension, cool extremities, elevated serum lactate level, and a low central venous pressure. The most appropriate immediate intervention is intravenous administration of a bolus of 10 mL/kg of an isotonic fluid such as normal saline, which directly addresses intravascular volume depletion and supports cardiac output. Oxygen supplementation (A) may improve saturation but does not correct the underlying hypovolemia or tissue hypoperfusion. Initiating intravenous epinephrine (C) could be appropriate if perfusion remains inadequate after fluid resuscitation, but starting vasoactive support before addressing preload is premature. Preparing for intubation (D) is unnecessary at this stage because the child is maintaining spontaneous respirations and airway protection. This 3-year-old child with congenital heart disease, severely decreased left ventricular function (ejection fraction of 25%), ongoing tachycardia, and tachypnea is demonstrating cardiogenic shock. The most appropriate next intervention is to intubate the child to provide mechanical ventilation support, which decreases the work of breathing, lowers oxygen consumption, and improves hemodynamic stability. Administering a rapid fluid bolus to a patient with poor left ventricular function risks worsening pulmonary edema, further compromising oxygenation (A). Initiating an intravenous norepinephrine infusion may increase afterload and myocardial oxygen consumption, which can exacerbate left ventricular dysfunction (B). Increasing the milrinone infusion rate is not appropriate here because it may worsen hypotension without improving forward blood flow in a patient in this decompensated state (C). This 10-year-old child with acute lymphoblastic leukemia presents with fever, hypotension, altered mental status, delayed capillary refill time, and elevated lactate level. All of these signs are consistent with septic shock in a patient with profound neutropenia (absolute neutrophil count <500/μL). The most appropriate immediate intervention is the administration of broad-spectrum intravenous antibiotics such as cefepime and vancomycin. Antibiotics should be started within 60 minutes in a patient with suspected sepsis to reduce morbidity and mortality. A norepinephrine infusion may be necessary if hypotension develops but should be started after fluid resuscitation (B). Corticosteroid administration can be considered to treat refractory shock after initial interventions are undertaken (C). Obtaining blood samples for culture is important but should never delay the initiation of empiric antimicrobial therapy in a patient with septic shock (D). AACN Certification Corporation publishes a study bibliography that identifies the sources from which items are validated. The document may be found in the AACN certification examination handbook. The contributor of each question written for this column has listed the source used in developing each item. Clinical practice should be based on primary sources of evidence when possible; this column will also include secondary sources to help nurses become aware of available resources for certification review.EBBERTSMarci Ebberts, MSN, APRN, FNP-C, CCRN, is the department editor. Marci is program director of nursing research at BJC West, Saint Luke’s, Kansas City, Missouri, and a practicing occupational health nurse practitioner. She welcomes feedback from readers and practice questions from potential contributors at ebberts.aprn@gmail.com.DERCHERLauren Dercher, MSN, RN, is an associate professor of nursing at Rockhurst University, Kansas City, Missouri, and a nurse on the medical intermediate cardiac care unit at Saint Luke’s Hospital, Kansas City, Missouri. Lauren collaborated with Marci Ebberts in writing the CCRN review questions.PELAYOOliver Lee Pelayo, MSN, RN, CCRN, TCRN, is a pediatric critical care nurse at Doernbecher Children’s Hospital, Oregon Health & Science University, Portland, Oregon. He collaborated with Serena Kelly in writing the pediatric CCRN review questions.KELLYSerena P. Kelly, MSN, CPNP-AC, FNP-BC, is an associate professor of pediatrics at Doernbecher Children’s Hospital, Oregon Health & Science University. Serena collaborated with Oliver Pelayo in writing the pediatric CCRN review questions.