IMG_6237

The words we use and the way we use words makes a difference. How we use words affects the way we think about the ideas and things that those words represent.

This idea is known as Linguistic Relativity or Whorfianism, named for Benjamin Whorf. The idea, in a general sense, is that the structure and vocabulary of a particular language affects the perception and cognitive processes of the speaker. A culture that doesn’t have a word for the concept of zero, for example, will develop different concepts and systems of mathematics than a culture with the word zero might. Having different words for shades of blue, like periwinkle, royal blue, or baby blue, will result in a greater cognitive perception of different shades of blue than might exist in a culture with only one word for blue. Moreover, having words for abstract concepts like love, honor, or justice, will transform the way ones perceives the world. Even the grammar and other semantic features of a language affect the way we think about things.

Noam Chomsky, of course, famously opposed Linguistic Relatively in favor of a more innate, biologic, Universal Grammar. Chomsky was so opposed to many of the ideas of Carl Jung that he rejected outright the idea that the language you speak and your vocabulary might influence your cognition, thoughts, and your behaviors. But today, most linguists appreciate that both the Universal and Relativistic schools have some validity, and Linguistic Relativity has had a resurgence in research in modern linguistic studies.

Suffice it to say, language affects the way we think. This connection cannot be understated when dealing with the cognitive biases that affect the way we treat patients. Let’s look at some examples.

A pregnant patient presents to the hospital for a complaint of decreased fetal movement at 33 weeks gestation. Her nonstress test is reassuring and she starts to feel movement as soon as she gets to the hospital. However, her blood pressures are elevated with readings of 152/94 and 146/91. She has no history of hypertension. The OB Resident orders a CBC, CMP, LDH, uric acid and a UA. An hour later those labs come back and the patient has a uric acid level of 4.2, normal liver enzymes, normal platelets, and trace proteinuria. Her blood pressures remain mildly elevated. The OB Resident calls the OB Attending. She tells her about the patient’s hypertension and then tells her that “her preeclampsia labs are normal so I think we can send her home and do a 24 hour urine collection for protein.” The Attending agrees.

This vignette is incredibly common. So what’s the problem? Just one word: “preeclampsia.” The truth is, the labs that were ordered add almost nothing to the question of whether or not the patient has preeclampsia. The labs tells us only that she doesn’t have HELLP syndrome. HELLP syndrome occurs in perhaps only 5% of patients who have preeclampsia. And while abnormal liver enzymes, serum creatinine, or platelets are recognized as possible signs of preeclampsia with severe features, these findings are present in less than 1 in 20 cases and even less often in asymptomatic patients. We won’t know whether the patient has preeclampsia until we see how much protein she spills per 24 hours.

So a better statement might have been “her HELLP labs are normal and, because her blood pressures are mild and she is asymptomatic, I think we can send her home to do a 24 urine collection.” Calling the labs “HELLP labs” rather than “preeclampia labs” reinforces the real reason for checking them and, in the revised statement, the decision to send her home is not because the “preeclampsia labs are normal” but because the has no signs or symptoms of severe features of preeclampsia. A subtle but important difference. Clarity is important. The student or resident who is learning from this experience gets two different lessons depending on which words are used that ultimately may reframe the way she diagnoses and treats this patient and future patients.

Other examples of this linguistic phenomenon might be “Amniotic Fluid Embolism” or “Meconium Aspiration Syndrome.” Our cognitive perceptions are profoundly influenced by the names of these clinical conditions. The name amniotic fluid embolism certainly seems to imply that the cause is related to embolizing amniotic fluid. As early as 1995, it was recognized that the true cause was similar to an anaphylactic, immune-mediated response, and the name Anaphylactoid Syndrome of Pregnancy was suggested as a replacement. Unfortunately, amniotic fluid embolism is so ingrained that the new name, 20 years later, has yet to catch on. But thinking of the syndrome as an anaphylactoid response has led to new treatments (like high dose steroids) and new avenues of research.

Similarly, the persistence of the name meconium aspiration syndrome (MAS) has stymied research and treatments of this clinical entity, which accounts for 2% of all perinatal deaths. Infants with the more severe, deadly version of the syndrome usually have persistent pulmonary hypertension. Of course, infants without meconium stained fluid may also suffer from persistent pulmonary hypertension. Classically, it was thought that the meconium, after being inhaled in the lungs of newborns, caused obstruction and/or a chemical pneumonitis that caused the shunting of blood causing the pulmonary hypertension.

This dogma (and the name which recursively defined the pathophysiology) led to decades of nonproductive treatments. For example, a common treatment approach for years was amnioinfusion, based on the idea that flushing out and diluting the amniotic fluid with infused saline would decrease the morbidity and mortality associated with MAS. But after years of this practice, based mainly on opinion and anecdote, definitive trials showed that it did not affect the outcomes of MAS; if anything, it increased the risk of things like chorioamnionitis. In other words, what made sense based on the bias that the name infers was actually harmful.

Another example of this was deep suctioning for MAS. Until about 2005, it was common practice to use a DeLee suction trap to suction out the infant below the laryngeal chords before the chest was delivered. In other words, once the head of the infant was delivered but before the chest, a tube was passed down and the airway was deep suctioned to prevent the baby from inhaling any meconium that might be there before the baby would take its first breath. But this practice too, when finally studied, made no difference in MAS outcomes and was potentially harmful, causing things like laryngeal spasm.

Newer evidence indicates that the pulmonary arterioles in infants who eventually die from MAS have undergone a process of thickening and increased muscularization that takes days to weeks to develop and is likely related to chronic antenatal stress or hypoxia. The same milieu of chronic stress and hypoxia in turn may also cause the fetal bowel movement in the first place. If it doesn’t, then the clinical diagnosis will be persistent pulmonary hypertension. If it does, the diagnosis will be MAS.

So, which came first, the pulmonary changes or the meconium? Undoubtedly, the meconium makes the pulmonary condition worse, but it may be a much smaller part of the picture than we once thought. But because it is called MAS, then our focus for decades has been on mechanically removing the meconium, using treatments that have been of no benefit and, indeed, potentially harmful. In fact, the most significant reduction in MAS has come from inducing women at 41 weeks rather than 42, leading to nearly a four-fold reduction in the number of cases. Why? Perhaps because of less chronic stress and hypoxia, and also probably less passage of meconium; but the rate of meconium stained amniotic fluid is only cut in half by induction at 41 weeks, yet the rate of MAS is decreased four-fold. So meconium, even if it is a factor, is probably a minor factor overall (see here if you think I’m crazy).

So our nomenclature matters. Research progress is slowed and treatments are incorrectly utilized because of how we name things. The way we teach is perverted. Whole concepts of certain diseases are cognitively distorted until we call them something different. Preeclampsia used to be called toxemia because we thought that menstrual toxins built up in the mother’s blood from months of not having periods, eventually leading to blood poisoning. This concept led to such brilliant treatments as blood-letting and leaches less than 100 years ago. What’s more, the idea that absent menstruation leads to build-up of dangerous blood toxins, as evidenced by toxemia, is the reason still today why some women think that it is unhealthy to use birth control methods that suppress menstruation. Words matter. Yet you still hear people use the term toxemia or the similarly out-dated term (since 1999) PIH or pregnancy-induced hypertension.

Phrases matter too. Our bias to believe that correlation equals causation has linguistic roots. If I say, “The patient was febrile until we treated her for pneumonia,” it is hard to intellectually escape the idea that the pneumonia was the cause of the fever. But this is an assumption which still needs to be tested. These kinds of potentially false connections are made every day in almost every conversation about every patient. They also drive anecdotal medicine. “I did x to a patient at risk of preterm delivery and she delivered at term” is as powerful an evidence that prevents preterm delivery as Andrew Wakefield’s paper showing that vaccines cause autism. Cause and effect bias is deeply ingrained in the syntax of our subject-verb-object language.

We can’t always change the way we say things, but we can be aware of the bias that it causes and point it out in our teaching.

By the way, you should order a CBC (for hemoglobin and platelets) and CMP (for creatinine and liver enzymes) for every patient that you diagnose with gestational hypertension, and each week thereafter until delivery.