Treating symptoms too soon may be the wrong idea
During our training, we learned little about colds because they are benign. However, upper respiratory infections are the number one diagnosis in primary care, which makes understanding how to treat them important. In the U.S., one billion cases of the common cold occur annually.
A friend told me he saw his doctor for a cold who issued a prescription for a newer, non-sedating, (and more expensive) antihistamine and an antibiotic. He didn't get any better; however, he did get heartburn from the antibiotic.
The virus itself does no damage. Symptoms from a cold are from our immune response, which drops the viral level to nearly zero by day five.
Runny nose and sneezing are beneficial; these defenses mechanically drain the infected area. Sneezing is brief, lasting only a few days and efforts to decrease sneezing and secretions will offset this benefit. Our immune system in response to infection generates chemical mediators, which contribute to fever. The most common cold virus, rhinovirus, doesn't like high temperatures thus medicines to decrease fever offset the benefit of the consequent low-grade fever. Nasal congestion also combats viral replication by raising the nasal temperature. Fever is not a prominent symptom in adults, which helps distinguish colds from influenza (as would cough at onset of disease). Incidentally, the term "influenza" is derived from the "influence" of the stars because it is seasonal.
Given that there is no medicinal agent that treats the underlying infection, interfering with the immune response, which does combat the infection, before day five would be counterproductive. After that, effective symptomatic relief requires an understanding of the mechanism. Work by Eccles and others contributed much to linking symptoms with their mediators.
Treatment of symptoms
A Sore throat is usually one of the first symptoms. Chemical messengers act at the sensory receptors of the pharynx, and topical anesthetic sprays blunt sensory nerve receptors in the pharynx. White blood cells produce chemical messengers. These chemicals cross the blood/brain barrier to the hypothalamus and produce different chemical messengers, which then change the thermal set point resulting in fever.
Antipyretics such as acetaminophen decrease these chemical messengers and so are used for fever, but as said, fever is usually mild and beneficial.
Normally, the nasal venous plexus dilates causing discrete occlusion every few hours on one side of the nose and then switches to the other side. This occurs to give the occluded side of the nose a chance to re-moisturize which improves the ability to smell. During a cold, this process is exaggerated by local chemical messengers and you can notice the congestion alternating.
The nasal passage normally drains moisture on the eye's surface down through your nose. The dilated nasal veins causing nasal congestion occlude this duct resulting in watery eyes.
White cells release chemicals, which break down muscle proteins. This causes pain, however for a greater good. The protein is converted by the liver to amino acid building blocks, which are then used to re-form different proteins as antibodies and complement proteins to fight the infection. Often NSAIDs are given, which decrease the chemical released by the white cells. NSAIDs hence decrease sore throat, fever, nasal congestion, watery eyes, and muscle pain
Runny nose (rhinorrhea)
Early (days 1-4), secretions derived from the nasal lining, are thin, and watery. This is mediated by an involuntary parasympathetic nerve, the vagus nerve; the neurotransmitter is acetylcholine. Early runny nose is treated with anticholinergic medicine.
After day four, secretions are instead from plasma exudate from capillaries, are thicker in viscosity, and not vagally mediated via acetylcholine. At this point, continued use of anticholinergic medicine for this symptom makes no sense. Kleenex makes more sense.
Nerves at the nasal lining travel to the brain stem then nerves descend from there to inspiratory/expiratory muscles. A separate set of nerves which are involuntary parasympathetic branches, activate facial muscle grimacing and nasolacrimal gland rhinorrhea upon sneezing. Nasal spray and antihistamines such as diphenhydramine are helpful at this point. Both the older and newer antihistamines bind the histamine receptor, but only the older, less expensive, sedating ones bind the acetylcholine receptor. Pseudoephedrine is abbreviated "D" for decongestant on labels. It augments the sympathetic limb via adrenaline and hence away from the parasympathetic acetylcholine limb. Pseudoephedrine can be modified to approximate an amphetamine for recreational use these days and is thus shelved away behind the counter
The virus binds to antibodies on mast type white blood cell membranes resulting in the release of histamine and consequent hives. You shall see this is the only symptom that involves histamine. Antihistamines, both old and new, block histamine receptors.
Secretions lead to pressure pain. Guaifenesin thins the viscosity of mucus to facilitate drainage of secretions; it is not a cough suppressant.
Much like sneezing, inflammatory mediators act on the sensory receptors at the larynx and below. The vagus nerve passes this signal to the brain stem and then nerves return to activate the respiratory muscles; the mechanism is via parasympathethic acetylcholine. (This reflex is also how gastroesophageal reflux, GERD, causes coughing). The cough can last up to three weeks. Less often, it can persist longer, termed "post infectious cough." Dextromethorphan abbreviated on labels as "DM" (not "D") acts at the brain stem to suppress cough and can therefore, be helpful. Opiates also suppress cough centrally at the brain stem and are stronger. Ipratropium oral inhalers block acetylcholine; the mediator of the parasympathetic nervous system which enacts cough.
Post infectious cough
This type of cough is the most prolonged symptom and so deserves more elaboration. Chronic cough is the single most common symptom of primary care visits. Persistence of inflammation can be the cause of or contribute to the cough. As is known, reclining increases GERD and post nasal drip and so can be a clue to a contributing mechanism of a predominantly nocturnal cough when prone. Further, consider that coughing from a cold can cause reflux, which can cause a more prolonged cough.
Also, a history of a "cold" (without nasal symptoms) and a visit for a cough, which was instead from the bacteria Mycoplasma, or Chlamydia may explain why the patient states, "The only thing that helped last time was an antibiotic."
Another misdiagnosis very much resembling the cold is pertussis. It is known as the hundred-day cough. It occurs during cold season, is highly contagious, starts with catarrhal symptoms, and is followed by a cough. The cough then worsens, characterized by post-tussive emesis, but typically doesn't have the whooping clue in adults. Like Mycoplasma and Chlamydia, pertussis also responds to macrolide type antibiotics. To be effective, the antibiotic is used early, during the first two weeks. The immunity to childhood DTaP series (Diphtheria, Tetanus, Pertussis) wanes so patients adolescent through age 64 should receive a (single) booster for pertussis to avert this scenario. (Patients aged 65 and older; predating DPT vaccines carry immunity from natural infection.) The Advisory Committee on Immunization Practices (ACIP) highlighted that adults anticipating contact with an unvaccinated infant should receive a Tdap booster. In 2010, the ACIP updated guidance that those aged 65 and older (who have not yet received a single booster) may also receive a booster. In a Canadian study of adults and adolescents, one-fifth of patients with postinfectious cough had pertussis.
Ipratropium oral inhalers have been advocated as first line treatment. Do consider if a component of the cough is from post-nasal drip, also from the ongoing inflammatory response, efficacy would be less than if post-nasal drip were also addressed. Inhaled steroids decrease inflammatory damage to the bronchiolar epithelium, but would also not address post-nasal drip. Oral steroid tablets, such as prednisone, suppress white cells that liberate the chemical messengers, which mediate symptoms and are elevated during cough. It is used for post infectious cough after three weeks (and for refractory hives). If used for the cough during infection, prednisone does not decrease cough, instead it increases the viral count.
Opiates act centrally. Because coughing itself can cause inflammation, opiates would break this cycle and are used for refractory post infectious cough.
This symptom is mediated directly from the chemicals released by white cells. As said, though prednisone does decrease white cell chemical messengers, when used during acute illness it raises the viral count.
Loss of appetite decreases expending energy for finding and digesting food. Also, eating less reduces the intake of bacterial growth factors as iron and zinc. This is the rationale behind the expression, "Starve a fever." Fevers in adults are higher in bacterial infections. Fever is not a prominent symptom in adults with colds (which are viral) and is then consistent with the folklore clause to instead, "Feed a cold" (however, viruses do, in fact, also utilize micronutrients for growth). Not eating and fever leads t dehydration, which thickens the viscosity of mucus. Take in plenty of fluids to balance dehydration.
Fatigue is mediated by the chemicals released by white cells. These chemicals result in "slowing down" thus conserving energy for healing. Rest is the best medicine for this symptom.
Better understanding averts meaningless treatment as well as lessens potential adverse drug effects and needless expense. Pertussis should be in the differential diagnosis of patients presenting with cold symptoms and providers should be aware that adult vaccinations now include a pertussis booster.
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"Treating symptoms too soon may be the wrong idea"
Dr. Musico was born in Beverly Hills, CA. His undergraduate work at USC included shark research in the Pacific and cancer research in Los Angeles. His clerkship included surgery in London, medicine in New York, and tropical medicine in the Windward I...