Polymyxin B — nephrotoxicity, neurotoxicity and the risk of respiratory paralysis

EFFECTIVE | TOXIC

Names under which Polymyxin B is found

The international nonproprietary name is polymyxin B; the active ingredient in medicinal products is usually presented as polymyxin B sulfate. One milligram of pure polymyxin B base corresponds to approximately 10,000 units. The systemic dosage form is a lyophilized powder for preparing a solution for intravenous, intramuscular, intrathecal, or ophthalmic use, usually containing 500,000 units per vial. In different countries, the drug may be marketed under the names Polymyxin B for Injection, Polymyxin B Sulfate, Aerosporin, and various local generic trade names.

Polymyxin B is included in numerous combination topical products: polymyxin B + trimethoprim — Polytrim and equivalents; neomycin + polymyxin B + dexamethasone — Maxitrol and equivalents; neomycin + polymyxin B + hydrocortisone — Cortisporin and equivalents; bacitracin + polymyxin B — Polysporin and equivalents; neomycin + polymyxin B — solutions, ointments, ophthalmic and otic formulations. These products cannot be considered interchangeable: their toxicological profile is determined not only by polymyxin B but also by other antibiotics, glucocorticosteroids, the route of administration, and the condition of the tissues. Particular attention should be paid to the simultaneous use of several ophthalmic, otic, wound-care, or irrigation products containing polymyxin B or other nephrotoxic and neurotoxic antibiotics.

Why Polymyxin B is considered harmless and where the real risk begins

Polymyxin B is often perceived as an “ordinary topical antibiotic” because many patients encounter it in eye drops, ear preparations, or ointments. However, systemic Polymyxin B is a drug with a narrow therapeutic range: the concentrations required to suppress a severe Gram-negative infection are dangerously close to those that damage the renal tubules and nervous system. The official prescribing information explicitly states that the drug can cause albuminuria, cylindruria, azotemia, paresthesias, ataxia, pronounced muscle weakness, apnea, and respiratory paralysis due to neuromuscular blockade.

A false sense of safety also arises because the early manifestations of toxicity are nonspecific. Drowsiness, dizziness, weakness, tingling around the mouth or in the extremities may be attributed to the infection, fever, hospitalization, or the effects of other medications. Reduced urine output may remain unnoticed for a long time, especially in a critically ill patient. Repeated doses can produce an accumulation effect, while impaired renal function increases the likelihood of high concentrations and pronounced neurotoxicity. Systemic Polymyxin B is not intended for self-treatment at home and should be used primarily for documented or reasonably suspected infections caused by susceptible Gram-negative bacteria when less toxic drugs are ineffective or contraindicated.

Side effects during the first hours and days of treatment

Common and relatively early reactions include dizziness, drowsiness, facial flushing, perioral paresthesias, numbness of the fingers and extremities, muscle weakness, soreness after intramuscular administration, and thrombophlebitis at the site of intravenous infusion. After intrathecal administration, chemical irritation of the meninges, fever, headache, neck stiffness, and increased cell count and protein levels in the cerebrospinal fluid may occur. Allergic reactions may present as drug fever, urticaria, and, much less commonly, systemic hypersensitivity.

Clinically significant early nephrotoxicity manifests as progressive azotemia, increased creatinine and urea levels, the appearance of protein and cellular casts in the urine, and reduced urine output. The damage predominantly affects the renal tubular epithelium. The absence of an immediate rise in creatinine does not rule out a toxic process: tubular abnormalities may begin before standard blood markers reflect a decline in filtration function. Post-marketing data have also described polymyxin-associated tubulopathy resembling pseudo-Bartter syndrome, with hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalcemia, and increased urinary potassium loss; creatinine may sometimes remain normal.

The most dangerous acute reaction is neuromuscular blockade. It may begin with increasing weakness, difficulty holding up the head, impaired swallowing, a weakened cough reflex, and shallow breathing, followed by hypoventilation or apnea. The risk is particularly high when the drug is administered soon after general anesthesia, during treatment with muscle relaxants, or in combination with other neurotoxic agents. In such a situation, further administration is stopped and respiratory support is provided immediately; waiting “until the drug leaves the body” may result in hypoxic brain injury or death.

Side effects with prolonged or repeated use

The main cumulative risk is acute kidney injury, the likelihood of which increases with treatment duration, total exposure, severity of illness, pre-existing kidney damage, age, dehydration, use of vasopressors, and combination with other nephrotoxic drugs. In clinical studies, nephrotoxicity during polymyxin therapy is common. After discontinuation, kidney function partially or completely recovers in many patients, but reversibility is not guaranteed: severe tubular injury may require renal replacement therapy, and in a patient with pre-existing chronic kidney disease it may result in a persistent decline in filtration.

Repeated and prolonged administration increases the risk of sensory and motor neurological disorders: persistent paresthesias, ataxia, muscle weakness, visual disturbances, psychomotor slowing, and episodes of neuromuscular blockade. The mechanisms of neurotoxicity are associated with damage to nerve-cell membranes, mitochondrial dysfunction, oxidative stress, and disruption of intracellular signaling pathways. Most neurological manifestations diminish after discontinuation, but in critically ill patients recovery may take days or weeks and depends on the level of exposure, renal function, concomitant medications, and the severity of hypoxia during respiratory failure.

Tolerance, psychological or physical dependence, and a classic withdrawal syndrome are not characteristic of Polymyxin B. The main problem with prolonged use is not dependence but selection of resistant strains, superinfection with nonsusceptible bacteria or fungi, and antibiotic-associated diarrhea, including Clostridioides difficile infection. This complication may occur not only during treatment but also more than two months after the course has been completed.

Contraindications and high-risk groups

A confirmed hypersensitivity to polymyxins is an absolute contraindication. Repeated administration after an allergic reaction may produce a faster and more severe response. The safety of systemic use during pregnancy has not been definitively established, so the drug is acceptable only for severe infection when the expected benefit outweighs the potential risk and there is no reliable safer alternative.

Patients with chronic kidney disease, baseline azotemia, oliguria, or acute kidney injury have less functional reserve and a higher risk of both further deterioration in renal function and neurotoxicity. At the same time, the modern pharmacokinetics of Polymyxin B are more complex than suggested by older prescribing information: renal clearance is not its primary route of elimination, so mechanically reducing the dose solely on the basis of estimated glomerular filtration rate may lead to inadequate antibacterial exposure. Dosing decisions should be based on the severity of infection, body weight, clinical course, therapeutic drug monitoring when available, and continuous assessment of toxicity rather than on independently “cutting the dose in half.”

Older patients, people with sepsis, shock, hypovolemia, dehydration, burns, multiple-organ failure, and patients receiving vasopressors are especially vulnerable. Their renal perfusion is already compromised, so additional tubular damage leads more quickly to clinically significant renal failure. After general anesthesia, in myasthenia gravis, other disorders of neuromuscular transmission, pronounced muscle weakness, or when muscle relaxants are required, the risk of neuromuscular blockade and respiratory paralysis increases sharply.

Topical, ophthalmic, and otic formulations usually produce substantially lower systemic exposure, but the risk increases when they are applied to extensive burn or wound surfaces, damaged mucous membranes, a bladder stripped of epithelium, a perforated tympanic membrane, or when prolonged irrigation is used. Under such conditions, systemic absorption with nephrotoxicity, ototoxicity, and neuromuscular blockade is possible, particularly in children, older adults, dehydrated patients, and those with impaired renal function.

Dangerous drug interactions

Combining Polymyxin B with curare-like muscle relaxants and agents that suppress neuromuscular transmission is contraindicated or highly undesirable. Succinylcholine, tubocurarine, gallamine, decamethonium, and certain anesthetics may add to presynaptic and postsynaptic impairment of impulse transmission, causing sudden respiratory failure. Administration of Polymyxin B soon after surgery is particularly dangerous when the clinical action of the muscle relaxant appears to have ended but residual blockade persists.

Simultaneous or sequential use with aminoglycosides is highly undesirable: gentamicin, tobramycin, amikacin, neomycin, streptomycin, kanamycin, and paromomycin. The combination increases renal tubular damage and neurotoxicity; for some combinations, the risks of ototoxicity and neuromuscular blockade also increase. Similar caution is required when combining Polymyxin B with colistin, bacitracin, and other polymyxins: there is usually no therapeutic benefit from duplicating toxic membrane-active antibiotics, while the toxicological burden is clearly additive.

Combinations with vancomycin, amphotericin B, cisplatin, tacrolimus, cyclosporine, high doses of loop diuretics, iodinated contrast agents, and other potentially nephrotoxic drugs require laboratory and clinical monitoring. The mechanism of interaction is predominantly pharmacodynamic: the renal tubules, microcirculation, and mitochondrial systems of renal cells are damaged simultaneously. If such agents cannot be discontinued, urine output, creatinine, urea, electrolytes, acid-base status, and overall changes in renal function must be monitored.

No clinically significant direct pharmacokinetic interaction of Polymyxin B with alcohol, caffeine, or nicotine has been established. However, alcohol can worsen dehydration, disrupt electrolyte balance, and mask drowsiness, ataxia, and impaired coordination — early signs of neurotoxicity. For a patient receiving systemic Polymyxin B for a severe infection, alcohol consumption has no rational justification. Dietary supplements and herbal products with potential nephrotoxicity, pronounced diuretic effects, or unknown composition are also undesirable because they may complicate interpretation of changes in creatinine, potassium, magnesium, and urine output.

Hidden duplication most often occurs not with systemic injections but when several combination ophthalmic, otic, dermatological, or wound-care products are used simultaneously. A patient may consider Polytrim, Maxitrol, Cortisporin, and Polysporin to be completely different medications, even though all of them may contain Polymyxin B. On small intact surfaces, systemic exposure is usually low, but with prolonged use, extensive tissue damage, or combination with systemic Polymyxin B, such polypharmacy should be identified and stopped.

Patient errors when using Polymyxin B

The most dangerous error is attempting to use the drug without microbiological confirmation that the pathogen is susceptible. Polymyxin B is not active against viruses, fungi, most Gram-positive bacteria, Gram-negative cocci, or bacteria of the Proteus group. Using it “just in case” does not provide universal antibacterial coverage, but it retains the nephrotoxic risk and creates selective pressure that promotes the spread of resistance.

The dose should not be increased independently, dosing intervals should not be shortened, and the treatment course should not be prolonged simply because there is no rapid effect. Treatment failure may be related to bacterial resistance, poor penetration of the drug into the infection site, inadequate drainage of an abscess, infection caused by a nonsusceptible pathogen, or irreversible organ damage during sepsis. Increasing exposure in such a situation primarily raises the likelihood of acute kidney injury and neurotoxicity rather than guaranteeing clinical success.

It is dangerous to ignore reduced urine output, sudden weakness, numbness around the mouth, tingling in the hands and feet, impaired balance, blurred vision, difficulty swallowing, or a sensation of insufficient air. These symptoms should not be attributed only to “severe infection” or general weakness after treatment. They may be the first manifestations of toxic injury to the nervous system or an emerging neuromuscular blockade. Continuing administration while waiting for a scheduled laboratory test increases the risk of apnea.

With topical use, common errors include instilling ear drops without ruling out perforation of the tympanic membrane, prolonged application of a combination ointment to a large wound or burn surface, using eye drops longer than prescribed, and simultaneously using several combination preparations. The presence of an antibiotic and a glucocorticosteroid in the same bottle particularly encourages self-treatment: redness temporarily decreases while a fungal, viral, or nonsusceptible bacterial infection may continue to progress.

Polymyxin B overdose and poisoning

A universal single toxic dose of Polymyxin B for humans has not been established. Toxicity depends not only on the amount administered but also on body weight, infusion duration, total exposure, renal function, critical illness, dehydration, age, concomitant nephrotoxic agents, anesthesia, and muscle relaxants. The official prescribing information limits the intravenous daily dose for patients with normal renal function to 25,000 units/kg, but remaining within the formal maximum does not rule out nephrotoxicity or neurotoxicity.

During the first hours of excessive exposure, facial flushing, dizziness, drowsiness, perioral numbness, “glove-and-stocking” paresthesias, blurred vision, impaired coordination, and muscle weakness may occur. As neuromuscular blockade intensifies, weakening of the voice, dysphagia, inability to take a deep breath, shallow breathing, rising carbon dioxide levels in the blood, loss of consciousness, and apnea may develop. After anesthesia, this process may progress more rapidly and be mistakenly interpreted as a residual effect of anesthesia.

Over the following hours and days, kidney injury may become predominant: reduced urine output, albuminuria, cylindruria, increased urea and creatinine, electrolyte losses, and metabolic alkalosis. Pronounced tubulopathy may cause hypokalemia and hypomagnesemia, which further worsen muscle weakness and create a risk of cardiac arrhythmias. Reduced urine output and rising urea are direct indications for discontinuing therapy according to the official prescribing information.

A hidden overdose may occur because of an error when converting milligrams to units: 1 mg of pure base corresponds to approximately 10,000 units. Additional sources of risk include incorrect determination of body weight, simultaneous prescription of systemic and intensive topical therapy, an incorrect infusion rate, repeat administration before the previous dose has been fully documented, and the use of different combination products containing Polymyxin B.

There is no specific antidote. If overdose is suspected, the drug is stopped immediately and respiration, blood gases, urine output, renal function, electrolytes, and acid-base status are monitored. In neuromuscular blockade, timely ventilatory support is vital. Severe kidney injury requires intensive correction of fluid and electrolyte abnormalities and, when indicated, renal replacement therapy, although this should not be regarded as a reliable method for rapidly removing the entire accumulated dose of Polymyxin B. Waiting for a marked rise in creatinine or complete respiratory arrest is unacceptable: both nephrotoxicity and neuromuscular blockade are more amenable to correction before irreversible damage develops.

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Safe integrative alternative and recovery after Polymyxin B

Polymyxin B cannot be replaced with herbal preparations in sepsis, bacteremia, hospital-acquired pneumonia, meningitis, and other severe infections caused by susceptible multidrug-resistant Gram-negative bacteria. In such situations, the drug is used not to reduce inflammation in general but to provide rapid bactericidal activity against a pathogen that directly threatens the patient’s life. A herbal alternative may be considered only for a mild or moderate uncomplicated inflammatory process when systemic infection, respiratory failure, severe intoxication, a purulent focus, central nervous system involvement, and rapid clinical deterioration have been ruled out.

As a basic herbal strategy for mild uncomplicated inflammation, a combination of Andrographis paniculata, Plu Kaow — Houttuynia cordata, Japanese honeysuckle, and Forsythia suspensa may be considered. Andrographis may serve as the central anti-inflammatory and immunomodulatory component, while Plu Kaow, Japanese honeysuckle, and forsythia may complement the combination in inflammatory conditions affecting the respiratory tract, mucous membranes, and urinary system.

When an intestinal or urogenital bacterial component is present, Chinese goldthread and common barberry may additionally be considered. Berberine-containing plants should not automatically be included for every patient: they have pronounced pharmacological activity and can affect intestinal motility, drug metabolism, and glucose levels. Cryptolepis buchananii may be considered as an additional antimicrobial component, but not as a substitute for a systemic antibiotic in sepsis or an infection caused by a carbapenem-resistant pathogen.

Purple coneflower, Astragalus propinquus, and common lungwort may be used as supportive components for immune, respiratory, and recovery support. They do not provide bactericidal activity in the blood and tissues comparable to Polymyxin B and should not be used to treat severe infection instead of adequate antibacterial therapy.

The main focus of an integrative approach after Polymyxin B is not only a possible herbal replacement for mild inflammation but also recovery after nephrotoxic and neurotoxic antibiotic therapy. Such recovery should begin not with aggressive forcing of diuresis or promises to “quickly eliminate the antibiotic,” but with monitoring of renal function, fluid balance, electrolytes, the intestinal barrier, mucous membranes, and the overall metabolic burden.

For urinary-system support after urine output has stabilized, Orthosiphon aristatus may be used. It is appropriate only when urine production is preserved, blood pressure is stable, and there is no pronounced dehydration. In oliguria, progressive elevation of creatinine, hypovolemia, hypokalemia, or hypomagnesemia, attempting to increase diuresis may worsen renal perfusion and electrolyte balance. Orthosiphon is not an antidote to Polymyxin B and does not replace monitoring of creatinine, urea, potassium, magnesium, acid-base status, and 24-hour urine output.

Additional antioxidant, anti-inflammatory, and hepatoprotective support may include milk thistle, turmeric, and Rehmannia glutinosa. These agents may support antioxidant systems, metabolic processes, and recovery after severe infection and combination drug therapy. They should not be presented as proven prevention of polymyxin-induced nephrotoxicity or as agents capable of reversing established renal tubular necrosis.

For restoration of the intestinal barrier, mucous membranes, and local immune defense after intensive antibiotic therapy, colostrum may be used. It contains immune and trophic components that may support the intestinal mucosa, but it does not replace diagnosis of antibiotic-associated diarrhea and Clostridioides difficile infection. Watery diarrhea, fever, abdominal pain, or blood in the stool requires evaluation for an infectious complication rather than treatment only with restorative products.

For antioxidant and metabolic support, polypore mushroom extract and Centella asiatica may additionally be used. Centella may also be included in recovery programs aimed at microcirculation and damaged tissues. Lion’s mane mushroom may reasonably be considered a component of trophic support for mucous membranes and the nervous system after the acute period has ended.

A metal and xenobiotic detoxification complex may be included after renal function has stabilized as part of support for natural metabolic and excretory systems. It should not be claimed that this complex directly binds Polymyxin B, acts as its antidote, or reliably accelerates elimination of the antibiotic. If oliguria, electrolyte disturbances, or acute kidney injury persist, any active detoxification programs should be postponed until the condition has stabilized.

Thus, an integrative strategy has two independent directions. The first is a herbal anti-inflammatory and antimicrobial alternative for a mild or moderate uncomplicated process in which Polymyxin B was not indicated in the first place. The second is restorative support after a necessary course of a reserve antibiotic: monitoring renal function and electrolytes, restoring the mucous membranes and intestinal barrier, reducing oxidative burden, and supporting microcirculation and the nervous system. These approaches must not be used instead of treatment for ongoing sepsis, bacteremia, or another severe infection.

Actual effectiveness of Polymyxin B and medical errors

Polymyxin B is genuinely effective against a number of susceptible Gram-negative bacteria, including certain multidrug-resistant strains of Pseudomonas aeruginosa, Acinetobacter baumannii, and carbapenem-resistant Enterobacterales. It binds to lipopolysaccharides and phospholipids in the bacterial outer membrane, disrupts its integrity, and produces rapid bactericidal activity.

The clinical value of Polymyxin B is greatest as a reserve drug when safer active antibiotics are unavailable, contraindicated, or inaccessible. It is not intended for treating the common cold, viral infections, inflammation without a bacterial pathogen, most Gram-positive infections, or conditions in which symptoms are caused not by infection but by allergy, autoimmune inflammation, or mechanical tissue injury.

Polymyxin B does not eliminate an abscess, necrotic tissue, an infected catheter, urinary tract obstruction, or another anatomical source of infection requiring drainage or surgical debridement. If the source of infection remains, increasing the antibiotic dose raises the risk of nephrotoxicity much faster than it increases the probability of clinical success.

Modern antibacterial therapy in many situations gives preference to newer β-lactam agents active against a specific resistance mechanism. Polymyxin B remains important, but the formula “a resistant Gram-negative bacterium was found, therefore a polymyxin is necessary” is too simplistic even for an on-call prescription. The location of the infection, susceptibility of the pathogen, minimum inhibitory concentration, penetration of the drug into the infection site, and availability of a safer alternative must all be considered.

For urinary tract infections, Polymyxin B is often not an optimal choice because it is eliminated predominantly by nonrenal pathways and does not produce a sufficiently predictable active concentration in the urine. Prescribing a nephrotoxic antibiotic that simultaneously fails to provide optimal urinary exposure is a remarkably effective way to worsen blood-test results without guaranteeing improvement in urine-test results.

Medical errors include prescribing the drug without culture and susceptibility testing, treating bacterial colonization instead of clinical infection, ignoring safer active antibiotics, incorrectly converting units to milligrams, errors in body-weight-based calculations, simultaneous use of several nephrotoxic drugs, and failure to monitor renal function daily.

No less dangerous is continuing treatment when urine output decreases, creatinine rises, hypokalemia develops, or perioral numbness, ataxia, or muscle weakness appears. Attempting to compensate for lack of effect by increasing the dose without reassessing the diagnosis, pathogen susceptibility, and source control primarily increases toxicity rather than the bactericidal wisdom of the prescription.

Safety monitoring during treatment

Before systemic therapy is started, creatinine, urea, estimated glomerular filtration rate, potassium, magnesium, sodium, calcium, bicarbonate or other measures of acid-base status, urinalysis, and baseline urine output should be determined. The presence of paresthesias, muscle weakness, ataxia, visual disturbances, swallowing problems, and breathing difficulties should be documented.

At the same time, the entire medication regimen should be reviewed. Whenever possible, aminoglycosides, vancomycin, amphotericin B, loop diuretics, calcineurin inhibitors, cytotoxic drugs, and other nephrotoxic or neurotoxic agents should be discontinued or replaced. If discontinuation is impossible, monitoring of renal function and electrolytes should be intensified.

In a critically ill patient, creatinine, urea, electrolytes, and urine output should be assessed daily. Creatinine is a delayed marker, so reduced urine production, the appearance of protein or casts in the urine, hypokalemia, hypomagnesemia, and metabolic alkalosis may indicate renal tubular injury earlier.

Acute kidney injury should be suspected if creatinine rises by at least 0.3 mg/dL within 48 hours, increases to 1.5 times or more above baseline within seven days, or urine output falls below 0.5 mL/kg/h for six hours. Such changes require immediate reassessment of dosing, concomitant therapy, and the need to continue Polymyxin B itself.

Increasing muscle weakness, perioral numbness, paresthesias, impaired coordination, blurred vision, difficulty swallowing, weakening of the voice, inability to take a deep breath, shallow breathing, pronounced drowsiness, hypoventilation, or apnea require emergency discontinuation of the drug and immediate evaluation. These signs may indicate neurotoxicity and neuromuscular blockade. If breathing is impaired, immediate respiratory support is required because waiting may lead to hypoxia and irreversible brain injury.

With topical, otic, or ophthalmic use, regular laboratory monitoring is usually unnecessary if the product is used for a short period and applied to a small intact surface. However, pronounced burning, swelling, rash, worsening vision, increased pain, impaired hearing, or lack of improvement require discontinuation of self-treatment and repeat diagnostic assessment. When applied to extensive burns, large wounds, or damaged mucous membranes, the possibility of systemic absorption must be taken into account.

Proper discontinuation and consequences of stopping treatment

Polymyxin B does not cause drug dependence and does not require gradual dose reduction. In nephrotoxicity, neurotoxicity, neuromuscular blockade, or a severe allergic reaction, the drug is discontinued immediately. Attempting to taper the dose of a toxic antibiotic does not prevent a withdrawal syndrome, because Polymyxin B does not cause one, but it does increase total toxic exposure.

In the absence of toxicity, treatment duration is determined by the location of the infection, type of pathogen, clinical response, and quality of source control. Independently stopping treatment once fever has subsided may lead to persistence of the pathogen, recurrence of bacteremia, and further selection of resistance.

At the same time, therapy should not be continued merely because a predetermined number of days was originally prescribed. If the infectious focus has been adequately managed, the clinical course is stable, and the necessary duration of therapy has been reached, additional doses do not automatically improve the outcome. An antibiotic should be used for as long as required to treat the infection, not until convincing laboratory evidence of toxicity appears.

If Polymyxin B is discontinued because of adverse reactions, an active alternative antibacterial therapy must be identified immediately. Simply stopping the drug without replacement while a severe infection persists may lead to recurrence of bacteremia, progression of sepsis, and multiple-organ failure.

After treatment is completed, renal function, electrolytes, and neurological symptoms should be monitored until sustained improvement is achieved. Creatinine may continue to rise after the last dose, while paresthesias and muscle weakness may persist for several days or weeks. Full recovery of renal function does not occur in all patients, especially those with pre-existing chronic kidney disease, septic shock, or exposure to several nephrotoxic drugs.

A rational approach to the use of Polymyxin B

Polymyxin B is justified in a severe confirmed infection caused by a susceptible multidrug-resistant Gram-negative pathogen when safer active drugs are unavailable or unsuitable. High toxicity does not make it useless: when the indication is correctly selected, the risk of kidney and nervous-system injury may be lower than the risk of death from an uncontrolled infection.

For mild or moderate uncomplicated inflammation, in the absence of systemic infection and a life-threatening bacterial process, using an antibiotic of last reserve is pharmacologically unjustified. After appropriate diagnostic assessment, a herbal strategy based on Andrographis paniculata, Plu Kaow, Japanese honeysuckle, and Forsythia suspensa may be considered in such situations.

After a necessary course of Polymyxin B, the priority is not to prescribe another set of potentially toxic drugs but to provide structured recovery. This includes monitoring renal function and electrolytes, correcting dehydration, restoring the intestinal barrier, providing antioxidant and anti-inflammatory support, normalizing nutrition, and gradually restoring damaged tissues.

Orthosiphon is appropriate only after urine output and electrolyte balance have stabilized. Milk thistle, turmeric, Rehmannia, colostrum, polypore mushroom extract, Centella asiatica, lion’s mane mushroom, and a metal and xenobiotic detoxification complex are selected individually, taking into account renal function, intestinal condition, concomitant medications, and the stage of recovery.

A rational integrative approach does not mean refusing effective antibacterial therapy or attempting to replace intensive-care treatment with herbal medicine. Its purpose is to avoid using Polymyxin B without strict indications, use the minimum necessary duration of treatment, detect toxicity in a timely manner, and, after the infection has been controlled, restore affected body systems with a lower medication burden.

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