Hyperglycemia in the ER - Guideline-Based Treatment Protocol (ADA 2026 / 2024 Consensus)

Step 1 - Immediate Assessment and Classification

Step 2 - Immediate Workup (Parallel with Treatment)

• Point-of-care: glucose, BHB (or urine ketones), venous blood gas
• Labs: BMP or CMP, magnesium, phosphorus, serum osmolality, CBC, urinalysis
• Calculated corrected sodium: Na + 1.6 × [(glucose - 100) / 100]
• Anion gap: Na - (Cl + HCO3) - normal is 8-12 mEq/L
• ECG - look for peaked T waves (hyperkalemia) before insulin
• Consider: blood cultures, lactate, troponin, lipase if precipitating cause unclear
• Identify precipitant: infection (most common), missed insulin, new-onset diabetes, MI, stroke, pancreatitis, medications (steroids, SGLT-2 inhibitors)

Step 3 - IV Fluids (Start Immediately)

DKA Fluid Protocol:

1. If hemodynamically unstable / shock: 1-2 L 0.9% NaCl or LR as fast as possible
2. After resuscitation: 250-500 mL/hr 0.9% NaCl or LR for first 4 hours, then reduce
3. When glucose <250 mg/dL: Switch to D5W + 0.45% NaCl at 150-250 mL/hr - this allows continued insulin infusion to close the anion gap
4. 2-bag method (preferred by many centers): Bag 1 (0.9% NaCl + KCl) and Bag 2 (D5W/0.9% NaCl + KCl) - mix ratio adjusted hourly based on glucose

HHS Fluid Protocol:

• Typically needs 8-10 L total deficit correction over 24-48 hours
• Start with 0.9% NaCl; switch to 0.45% NaCl once corrected sodium is normal
• Add dextrose when glucose <300 mg/dL
• Rate of glucose decline: do not exceed 90-120 mg/dL/hour
• Rate of serum sodium decline: do not exceed 10 mmol/L over 24 hours
• Osmolality decline: do not exceed 3-8 mOsm/kg/hour (to prevent cerebral edema)

Step 4 - Potassium Replacement (BEFORE starting insulin if K <3.5)

Step 5 - Insulin Therapy

Severe/Moderate DKA and HHS (ADA 2026 Recommendation 16.16 - Grade A):

1. Fixed-rate IV infusion: Regular insulin at 0.1 units/kg/hour (max 15 units/hour)
   • Optional: 0.1 units/kg IV bolus if there will be a delay in starting the infusion
2. Nurse-driven variable rate protocol: titrate based on glucose values; minimum rate 1 unit/hour (to ensure acidosis resolution in DKA)
3. Co-administer basal insulin early (e.g., glargine 0.1-0.125 units/kg SC q12h): New in 2024/2025 guidance - reduces rebound hyperglycemia without increasing hypoglycemia risk

• DKA: Target 150-200 mg/dL while anion gap is open
• HHS: Target 250-300 mg/dL initially (slower correction to prevent neurologic complications)

Mild/Uncomplicated DKA (NEW - ADA 2024/2025):

• Lispro or aspart 0.2-0.3 units/kg SC, then 0.1 units/kg SC every 1-2 hours until resolution

Step 6 - Transition from IV to SC Insulin (Critical Step)

1. Administer basal insulin (glargine/detemir) 2-4 hours BEFORE stopping the IV infusion
2. If the patient was on insulin at home, restart their home regimen
3. If insulin-naive, initiate total daily dose (TDD) of 0.5-0.8 units/kg/day split 50% basal / 50% prandial

• Glucose <200 mg/dL (DKA) or <250-300 mg/dL (HHS)
• Anion gap ≤12 mEq/L
• Venous pH >7.30
• BHB <0.6 mmol/L OR bicarbonate ≥18 mEq/L
• Patient able to eat

Step 7 - Other Electrolytes and Bicarbonate

• Severe acidosis: venous pH <6.9
• Life-threatening hyperkalemia (K >6.5 with ECG changes)
• Cardiovascular collapse

• Serum phosphate <1.0 mg/dL
• Cardiac dysfunction, hemolytic anemia, or respiratory compromise

Step 8 - Monitoring Schedule

Step 9 - Simple Hyperglycemia Without Crisis (Glucose 200-600, pH Normal, No Ketones)

• IV fluids for dehydration
• Correction dose of SC rapid-acting insulin (1 unit per 50 mg/dL above goal, adjusted by insulin sensitivity)
• If no known diabetes: work up for new-onset DM; avoid aggressive insulin without glucose monitoring
• Stress hyperglycemia (e.g., post-MI, sepsis): maintain glucose 140-180 mg/dL per ADA inpatient targets
• Do not discharge without arranging follow-up and education

Step 10 - Discharge Planning (ADA 2026 Recommendation 16.17 - Grade B)

• Identify and document the precipitating cause
• Education on sick-day rules, DKA prevention, insulin adjustment
• Reconcile and update insulin regimen
• Early endocrinology follow-up within 1-2 weeks
• Consider CGM referral

Quick Reference Summary

Paraquat Poisoning - Detailed Overview and Treatment

What is Paraquat?

Routes of Exposure

Mechanism of Toxicity

1. Paraquat (PQ²⁺) accepts a single electron from NADPH-cytochrome P450 reductase, xanthine oxidase, NADH-ubiquinone reductase, or nitric oxide synthase, becoming a paraquat radical cation (PQ·⁺)
2. PQ·⁺ rapidly donates its electron to molecular oxygen, generating superoxide radical (O₂·⁻)
3. Superoxide undergoes further reactions to produce hydrogen peroxide and - via the Fenton reaction (iron-dependent) - the highly reactive hydroxyl radical (OH·)
4. These reactive oxygen species cause lipid peroxidation, degrading cell membranes, causing cell dysfunction and necrosis
5. Paraquat also inhibits superoxide dismutase, the enzyme that normally scavenges superoxide
6. This redox cycle is self-regenerating - paraquat is not consumed; it just keeps cycling and generating ROS

Why the Lung is the Target Organ:

• Lung alveolar type I and II cells actively concentrate paraquat against a concentration gradient via a polyamine uptake transporter (energy-dependent)
• Lung tissue achieves paraquat concentrations 6-10x higher than plasma
• The high ambient oxygen tension in the lung accelerates the redox cycle
• Oxygen supplementation worsens lung injury - this is a critical clinical point

Biphasic Lung Injury

• Loss of type I alveolar cells (gas exchange impairment)
• Loss of type II alveolar cells (surfactant production impairment)
• Hemorrhage and inflammatory cell infiltration
• Pulmonary edema / ARDS-like picture
• Potentially reversible at this stage

• Fibroblast proliferation
• Interstitial and alveolar fibrosis
• Rapid progressive respiratory failure
• Usually irreversible
• Death from ventilatory failure in days to weeks

Clinical Staging (Tintinalli's Emergency Medicine)

Clinical Features - Timeline

Immediate (0-24 hours):

• Oral/GI corrosion: burning sensation of lips, mouth, pharynx; painful ulcers of oral mucosa, tongue, pharynx, esophagus within 1-2 days
• Nausea, vomiting (may be profuse), diarrhea, hematemesis, bloody stools
• Abdominal pain, buccopharyngeal pain
• Hypovolemia from GI losses
• Oropharyngeal ulcers (characteristic "paraquat stomatitis")

Days 1-5:

• Acute kidney injury: earliest and most important early marker; oliguria, rising creatinine and urea
• Hepatotoxicity: elevated bilirubin, ALT/AST, alkaline phosphatase; hepatic necrosis
• Pancreatitis (especially with large ingestions)
• Metabolic lactic acidosis
• Adrenal necrosis
• Myocardial injury / toxic myocarditis

Days 5 onwards - Weeks:

• Progressive pulmonary fibrosis - the dominant cause of death in survivors of the acute phase
• Worsening dyspnea, cough, hemoptysis
• Pleural effusions
• Refractory hypoxemia (PaO₂ drops progressively)
• Restrictive ventilatory pattern (reduced compliance, reduced DLCO)
• Death from ventilatory failure

Diagnosis

Clinical History:

• Exposure to paraquat (agricultural setting, suicidal ingestion)
• Characteristic oral ulcers after ingestion

Urine Dithionite Test (Bedside, Quick):

• Add 1 mL urine + a few drops of 1% sodium dithionite in 1M NaOH
• Blue/blue-green color = paraquat present (positive)
• Sensitivity decreases with time and dilution; negative does not exclude toxicity

Plasma Paraquat Level:

• Quantitative plasma levels correlated with time post-ingestion predict survival (Proudfoot nomogram)
• Levels drawn at specific times post-ingestion stratify risk
• Rising creatinine is a key marker: increase >0.049 mg/dL/hour over 6 hours = poor prognosis; associated with death

Serum Lactate:

• Lactate >3.35 mmol/L: 74% sensitivity for mortality
• Lactate >4.4 mmol/L: 82% sensitivity for mortality

Laboratory:

• BMP/CMP: AKI (BUN, creatinine), hepatic injury (bilirubin, LFTs)
• ABG: metabolic acidosis, falling PaO₂
• Serum cystatin C: rise >0.009 mg/L over 6 hours = associated with death
• Serum amylase/lipase (pancreatitis)
• CBC, coagulation studies
• Serum trypsin inhibitor (depressed in lung damage - forensic marker)

Imaging:

• CXR: diffuse pulmonary infiltrates; may be normal early
• CT chest: ground-glass opacities, consolidation, pleural effusion, evolving fibrosis - used to track proliferative phase and guide prognosis

Treatment - Step by Step

There is NO specific antidote for paraquat.

Step 1 - Immediate Gastrointestinal Decontamination (CRITICAL - Must be done ASAP)

• Fuller's Earth (hydrated aluminum silicate): 150 g in 200 mL water orally, repeat with 50 g every 4 hours for 3 doses - binds paraquat very effectively
• Activated Charcoal: 1-2 g/kg orally if Fuller's Earth unavailable; effective adsorbent
• Bentonite-magma (4-7% solution): stomach wash and leave some in stomach (per Dikshit's Forensic Medicine)
• Both Fuller's Earth and activated charcoal are considered standard; neither is clearly superior

Step 2 - Prevent Systemic Absorption and Enhance Elimination

• Aggressive fluid resuscitation for hypovolemia from GI losses
• Forced diuresis: high urine output helps excrete absorbed paraquat via kidneys as early as possible

Step 3 - Extracorporeal Elimination (2026 Evidence: Yang et al., Ann Med 2026)

Step 4 - Immunosuppression (Widely Practiced, Evidence Still Debated)

• Methylprednisolone (pulse): 1 g IV daily for 3 days, then taper; OR
• Dexamethasone: 8-16 mg IV daily
• Cyclophosphamide: 15 mg/kg IV (typically 750 mg-1 g) for 2-3 days

• Lin et al. (RCT): reduced mortality with cyclophosphamide + methylprednisolone
• Subsequent studies: improved survival with repeated pulse methylprednisolone + cyclophosphamide + dexamethasone
• Gawarammana RCT: high-dose cyclophosphamide vs. placebo showed no mortality difference, but suggested possible benefit with steroids
• Many earlier positive trials were stopped prematurely (Type I error risk)
• Bottom line: Evidence is mixed. Benefits appear most likely in the severe (not fulminant) group. Widely practiced despite lack of definitive RCT evidence. Should be initiated early.

Step 5 - Antioxidant Therapy

• N-Acetylcysteine (NAC): 150 mg/kg IV over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours (same dosing as acetaminophen toxicity) - widely used; free radical scavenger, glutathione precursor
• Vitamin C (Ascorbic acid): 2-3 g IV daily - antioxidant
• Vitamin E (Tocopherol): 400-800 IU daily - lipid-soluble antioxidant, membrane-protective
• Salicylate: Anti-inflammatory, NF-kB inhibitory actions

Step 6 - Oxygen Management (CRITICAL - Counterintuitive)

• Paraquat and oxygen have synergistic toxicity - high O₂ concentrations sustain the redox cycle and accelerate lung injury
• Target SpO₂: 88-92% (permissive hypoxemia; tolerate low-normal O₂ levels)
• Only use supplemental O₂ if SpO₂ <85% or patient is in severe respiratory distress
• Use the minimum FiO₂ needed to maintain SpO₂ ≥88%
• This is one of the most critical and counterintuitive aspects of paraquat management

Step 7 - Respiratory Support

• As pulmonary fibrosis progresses, mechanical ventilation is often required
• Low tidal volume ventilation (6 mL/kg ideal body weight) - lung protective
• Minimize FiO₂ as above
• PEEP as needed for oxygenation while keeping FiO₂ low
• Prone positioning if refractory hypoxemia
• ECMO has been used in selected cases as a bridge; very limited data

Step 8 - Renal Support

• Monitor urine output, creatinine, cystatin C hourly-2 hourly
• Aggressive early IV hydration to maintain urine output ≥1-2 mL/kg/hour
• CRRT preferred over HD for both renal support and paraquat removal once AKI develops
• Avoid nephrotoxic drugs

Step 9 - General Supportive Care

• Oral care: meticulous oral hygiene; chlorhexidine mouthwash for painful oral ulcers; topical anesthetics
• Nutrition: early enteral nutrition if GI tract permits; parenteral nutrition if severe GI corrosion
• Analgesia: opioids may be needed for severe mucosal pain
• Infection control: immunosuppressive therapy increases infection risk; monitor and treat proactively
• GI protection: proton pump inhibitors for esophageal/GI ulceration
• Corticosteroid adrenal support: adrenal necrosis can cause adrenal insufficiency

Step 10 - Organ Transplantation

• Lung transplantation has been attempted in a small number of cases
• Only considered when the systemic paraquat burden is completely eliminated (confirmed by undetectable plasma/urine levels) to prevent transplanted lung injury
• Very few centers offer this and outcomes remain poor
• Not a practical option in most settings

Prognosis

• Ingested volume >20 mg/kg (>7.5 mL of 20% solution)
• Age >50 years
• Pre-existing renal disease
• Plasma paraquat level above the Proudfoot nomogram threshold
• Creatinine rise >0.049 mg/dL/hour over 6 hours
• Lactate >4.4 mmol/L
• Early onset of respiratory failure (<48 hours)
• Positive urine dithionite test in high concentration

Summary Treatment Algorithm

Ingestion confirmed
      |
      ▼
IMMEDIATE: Fuller's Earth / Activated Charcoal (within 1-2 hrs)
+ IV fluids, airway assessment
      |
      ▼
LABS: Urine dithionite test, plasma paraquat, BMP, ABG, 
      lactate, LFTs, CBC, cystatin C
      |
      ▼
SEVERITY STRATIFICATION (Tintinalli criteria)
      |
   ┌──┴──┐
 Mild   Severe/Fulminant
   |         |
Monitor   EXTRACORPOREAL THERAPY:
           HP within 4-6 hrs (preferred)
           HP + CRRT if AKI develops
           AVOID HD as primary method
              |
              ▼
           IMMUNOSUPPRESSION:
           Methylprednisolone 1g/day x3d +
           Cyclophosphamide 15 mg/kg x2-3d
              |
              ▼
           ANTIOXIDANTS: NAC, Vit C, Vit E
              |
              ▼
           OXYGEN RESTRICTION: SpO₂ 88-92%
              |
              ▼
           RESPIRATORY SUPPORT: LPV if ventilated
              |
              ▼
           RENAL: CRRT, urine output monitoring
              |
              ▼
           SUPPORTIVE: oral care, nutrition, 
           GI protection, infection surveillance

Paraquat Poisoning - Detailed Overview and Treatment

What is Paraquat?

Routes of Exposure

Mechanism of Toxicity

1. Paraquat (PQ²⁺) accepts a single electron from NADPH-cytochrome P450 reductase, xanthine oxidase, NADH-ubiquinone reductase, or nitric oxide synthase, becoming a paraquat radical cation (PQ·⁺) [1]
2. PQ·⁺ rapidly donates its electron to molecular oxygen, generating superoxide radical (O₂·⁻) [2]
3. Superoxide undergoes further reactions to produce hydrogen peroxide and - via the Fenton reaction (iron-dependent) - the highly reactive hydroxyl radical (OH·) [6]
4. These reactive oxygen species cause lipid peroxidation, degrading cell membranes, causing cell dysfunction and necrosis [2]
5. Paraquat also inhibits superoxide dismutase, the enzyme that normally scavenges superoxide [3]
6. This redox cycle is self-regenerating - paraquat is not consumed; it just keeps cycling and generating ROS [2,6]

Why the Lung is the Target Organ:

• Lung alveolar type I and II cells actively concentrate paraquat against a concentration gradient via a polyamine uptake transporter (energy-dependent) [2,6]
• Lung tissue achieves paraquat concentrations 6-10x higher than plasma [3]
• The high ambient oxygen tension in the lung accelerates the redox cycle [6]
• Oxygen supplementation worsens lung injury - this is a critical clinical point [3,6]

Biphasic Lung Injury [2,6]

• Loss of type I alveolar cells (gas exchange impairment)
• Loss of type II alveolar cells (surfactant production impairment)
• Hemorrhage and inflammatory cell infiltration
• Pulmonary edema / ARDS-like picture
• Potentially reversible at this stage

• Fibroblast proliferation
• Interstitial and alveolar fibrosis
• Rapid progressive respiratory failure
• Usually irreversible
• Death from ventilatory failure in days to weeks

Clinical Staging [2]

Clinical Features - Timeline

Immediate (0-24 hours) [1,2]:

• Burning sensation of lips, mouth, pharynx; painful ulcers of oral mucosa, tongue, pharynx, esophagus within 1-2 days
• Nausea, vomiting (may be profuse), diarrhea, hematemesis, bloody stools
• Abdominal pain, buccopharyngeal pain
• Hypovolemia from GI losses
• Oropharyngeal ulcers (characteristic "paraquat stomatitis")

Days 1-5 [2,3]:

• Acute kidney injury: earliest and most important early marker; oliguria, rising creatinine and urea
• Hepatotoxicity: elevated bilirubin, ALT/AST, alkaline phosphatase; hepatic necrosis
• Pancreatitis (especially with large ingestions)
• Metabolic lactic acidosis
• Adrenal necrosis
• Myocardial injury / toxic myocarditis

Days 5 onwards - Weeks [2,3,6]:

• Progressive pulmonary fibrosis - the dominant cause of death in survivors of the acute phase
• Worsening dyspnea, cough, hemoptysis
• Pleural effusions
• Refractory hypoxemia (PaO₂ drops progressively)
• Restrictive ventilatory pattern (reduced compliance, reduced DLCO)
• Death from ventilatory failure

Diagnosis

Clinical History:

• Exposure to paraquat (agricultural setting, suicidal ingestion) [2]
• Characteristic oral ulcers after ingestion [1]

Urine Dithionite Test (Bedside, Quick) [2]:

• Add 1 mL urine + a few drops of 1% sodium dithionite in 1M NaOH
• Blue/blue-green color = paraquat present (positive)
• Sensitivity decreases with time and dilution; negative does not exclude toxicity

Plasma Paraquat Level [2,3]:

• Quantitative plasma levels correlated with time post-ingestion predict survival (Proudfoot nomogram)
• Levels drawn at specific times post-ingestion stratify risk

Prognostic Markers [2]:

• Creatinine rise >0.049 mg/dL/hour over 6 hours - associated with death [2,7]
• Cystatin C rise >0.009 mg/L over 6 hours - associated with death [2]
• Lactate >3.35 mmol/L: 74% sensitivity for mortality [2]
• Lactate >4.4 mmol/L: 82% sensitivity for mortality [2]

Laboratory [1,2]:

• BMP/CMP: AKI (BUN, creatinine), hepatic injury (bilirubin, LFTs)
• ABG: metabolic acidosis, falling PaO₂
• Serum amylase/lipase (pancreatitis)
• CBC, coagulation studies
• Serum trypsin inhibitor (depressed in lung damage)

Imaging [3]:

• CXR: diffuse pulmonary infiltrates; may be normal early
• CT chest: ground-glass opacities, consolidation, pleural effusion, evolving fibrosis - used to track proliferative phase and guide prognosis

Treatment

There is NO specific antidote for paraquat [1,2,3]. All treatment is directed at reducing absorption, enhancing elimination, slowing lung injury, and supportive care.

Step 1 - Immediate Gastrointestinal Decontamination [1,2,3]

• Fuller's Earth (hydrated aluminum silicate): 150 g in 200 mL water orally, repeat with 50 g every 4 hours for 3 doses
• Activated Charcoal: 1-2 g/kg orally if Fuller's Earth unavailable
• Bentonite-magma (4-7% solution): stomach wash and leave some in stomach [1]

Step 2 - IV Fluids and Forced Diuresis [1]

• Aggressive fluid resuscitation for hypovolemia from GI losses
• Forced diuresis: high urine output helps excrete absorbed paraquat renally as early as possible

Step 3 - Extracorporeal Elimination [4,8]

Step 4 - Immunosuppression [5,9]

• Methylprednisolone (pulse): 1 g IV daily for 3 days, then taper; OR
• Dexamethasone: 8-16 mg IV daily
• Cyclophosphamide: 15 mg/kg IV (750 mg-1 g) for 2-3 days

Step 5 - Antioxidant Therapy [3]

• N-Acetylcysteine (NAC): 150 mg/kg IV over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours
• Vitamin C (Ascorbic acid): 2-3 g IV daily
• Vitamin E (Tocopherol): 400-800 IU daily
• Salicylate: Anti-inflammatory, NF-kB inhibitory actions

Step 6 - Oxygen Management - CRITICAL [2,3,6]

• Do NOT give supplemental oxygen unless absolutely necessary
• Paraquat and oxygen have synergistic toxicity; high FiO₂ accelerates the redox cycle and worsens lung injury [2,6]
• Target SpO₂: 88-92% (permissive hypoxemia)
• Only supplement O₂ if SpO₂ <85% or severe respiratory distress
• Use the minimum FiO₂ needed to maintain SpO₂ ≥88%

Step 7 - Respiratory Support [6]

• Low tidal volume ventilation (6 mL/kg IBW) - lung protective strategy
• Minimize FiO₂ at all times
• PEEP titrated for oxygenation while keeping FiO₂ low
• Prone positioning for refractory hypoxemia
• ECMO as a bridge in selected cases (very limited data)

Step 8 - Renal Support [4]

• Monitor urine output, creatinine, cystatin C every 1-2 hours during active phase
• Aggressive IV hydration to maintain urine output ≥1-2 mL/kg/hour
• CRRT preferred over HD once AKI develops (both for renal support and paraquat removal)
• Avoid nephrotoxic agents

Step 9 - General Supportive Care [1,2]

• Oral care: chlorhexidine mouthwash; topical anesthetics for paraquat stomatitis
• Nutrition: early enteral nutrition if GI tract permits; parenteral if severe GI corrosion
• Analgesia: opioids for severe mucosal pain
• Infection surveillance: immunosuppression increases infection risk
• GI protection: proton pump inhibitors for esophageal and GI ulceration
• Adrenal support: adrenal necrosis can cause adrenal insufficiency

Step 10 - Lung Transplantation [2,3]

• Attempted in a small number of cases
• Only considered when systemic paraquat burden is completely eliminated (undetectable plasma/urine levels) to prevent transplanted lung re-injury
• Very few centers; outcomes remain poor

Prognosis

• Ingested volume >20 mg/kg (>7.5 mL of 20% solution)
• Age >50 years
• Pre-existing renal disease
• Plasma paraquat level above Proudfoot nomogram threshold
• Creatinine rise >0.049 mg/dL/hour over 6 hours
• Cystatin C rise >0.009 mg/L over 6 hours
• Lactate >4.4 mmol/L
• Early respiratory failure (<48 hours)

References

1. Dikshit PC. Textbook of Forensic Medicine and Toxicology. New Delhi: Peepee Publishers; 2007. Chapter: Paraquat Poisoning; p. 570.
2. Tintinalli JE, Ma OJ, Yealy DM, Meckler GD, Stapczynski JS, Cline DM, et al. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 10th ed. New York: McGraw-Hill; 2023. Chapter 201: Bipyridyl Herbicides; p. 1347-1349.
3. Murray JF, Broaddus VC, Ernst JD, King TE, Lazarus SC, Nadel JA, et al., editors. Murray & Nadel's Textbook of Respiratory Medicine. 7th ed. Philadelphia: Elsevier; 2022. Chapter: Paraquat; p. 998-1003.
4. Yang B, Ye D, Zeng F, Jiang Z, Li H, Liu N. Extracorporeal therapies in the management of paraquat poisoning: a comprehensive review of current evidence. Ann Med. 2026;58(1):2621498. doi: 10.1080/07853890.2026.2621498. PMID: 41612945.
5. Havaldar AA. Successful management of paraquat poisoning: a case report. J Med Case Rep. 2025 Oct 3;19(1). doi: 10.1186/s13256-025-05546-y. PMID: 41044637.
6. Katzung BG, editor. Basic and Clinical Pharmacology. 16th ed. New York: McGraw-Hill; 2024. Chapter: Bipyridyl Herbicides; p. 1578.
7. Huang W, Zhang Z, Lu YQ. Serum creatinine in predicting mortality after paraquat poisoning: a systematic review and meta-analysis. PLoS One. 2023;18(2):e0281897. doi: 10.1371/journal.pone.0281897. PMID: 36812192.
8. Eizadi-Mood N, Jaberi D, Barouti Z, Rahimi A, Mansourian M, Dorooshi G. The efficacy of hemodialysis on paraquat poisoning mortality: a systematic review and meta-analysis. J Res Med Sci. 2022;27:77. doi: 10.4103/jrms.jrms_235_21. PMID: 36353345.
9. Zhang X, Li T, Lu YQ. Mesenchymal stem cell-based therapy for paraquat-induced lung injury. Cell Biol Toxicol. 2024;40(1):75. doi: 10.1007/s10565-024-09911-3. PMID: 39136896.